rev 2019 kasbp fall symposium program final

Invitation Letter

Korean American Society in Biotech and Pharmaceuticals (KASBP) invites you to the

“2019 KASBP Fall Symposium” in Boston from November 1 to November 2, 2019. This

Fall Symposium focuses on “Current Trends in Key Therapeutic Approaches” and is co-

hosted by Daewoong Pharmaceuticals with our honorable sponsors, LG Chem, Samsung

Biologics, KHIDI, KRIBB and KPBMA.

The symposium organizing committee has recruited outstanding speakers and panelists,

including our distinguished keynote speaker, Dr. Kwang-Soo Kim, Professor of

Psychiatry and Neuroscience, Harvard Medical School. We are delighted to announce

that Dr. Kim is selected as the recipient of “KASBP-Daewoong Achievement Award” for

his long-standing contribution to major brain disorders.

Six distinguished speakers are invited from industry who will share their experience and

expertise regarding cutting-edge science, process from the early discovery research to

the clinical trials and new trends in drug discovery. They will present the drug discovery

challenges and technology in the diverse fields such as Immuno-oncology, Idiopathic

pulmonary fibrosis, Ophthalmology, Infectious diseases and Artificial intelligence.

We are also delighted to announce that awardees will be selected for KASBP-Daewoong,

KASBP-LG Chem, KASBP-Samsung Biologics, KASBP-KRIBB and KASBP Fellowship

respectively, which is possible by generous contribution of our sponsors.

Job fair also became a long tradition of KASBP symposium program, and many qualified

applicants will have an opportunity to interview with prominent Korean pharmaceutical

and biotechnology companies.

With these exciting topics and themes, the symposium organizing committee is looking

forward to meeting all members and friends in Boston!

November 1st, 2019

2019 KASBP Fall Symposium Organizing Committee

Program Chair Hyun-Hee Lee

KASBP President K. Stephen Suh

2019 KASBP Fall Symposium Program

2 |P a g e 2 0 1 9 K A S B P F a l l S y m p o s i u m

2019 – 2020 KASBP OFFICERS

Title Name 한글 이름 Affiliation

President K. Stephen Suh 서광순 DiagnoCine

President Designated Soo-Hee Park 박수희 Novartis

1st Vice President Wooseok Han 한우석 Novartis

2nd Vice President Hyun-Hee Lee 이현희 Merck

Executive Director Hanjo Lim 임한조 Genentech

General Director Sungkwon Kim 김성권 Alexion

Fellowship Director Hakryul Cho 조학렬 Agios

Technology Director Hyunjin Shin 신현진 Takeda

Financial Director Sahee Kim 김사희 RevHealth, LLC

Web Director DaeHo Lee 이대호 Express Care Pharmacy

Career development Director Dooyoung Lee 이두영 Morphic Therapeutic

Member Networking Director Sandy Suh 서샌디 Exeltis

Membership Director Sungki Kim, Hyelim Kim 김성기, 김혜림 MCPHS University

Public Relations Director Kern Chang 장건희 Janssen

YG Director Ji Eun Lee 이지은 MCPHS University

Legal Director Elizabeth Lee 이엘리자베스 Lucas & Mercanti

Graphic Designer Jiyoung Park 박지영 Golden Healthcare Pharmacy

NJ Chapter President Jae-hun Kim 김재훈 IFF

Boston Chapter President Soo-Hee Park 박수희 Novartis

Connecticut Chapter President Sung-Kwon Kim 김성권 Alexion

Philadelphia Chapter President Younghoon Oh 오영훈 Spark Therapeutics

San Francisco Chapter President Hanjo Lim 임한조 Genentech

Washington DC Chapter President Nam Cheol Kim 김남철 United States Pharmacopeia

Illinois Chapter President Seungwon Chung 정승원 AbbVie

Councilor – Finance/legal Yun H. Choe 최윤 Lucas & Mercanti

Councilor - Grant Hak-Myung Lee 이학명 Shire

Councilor - Auditing Sungtaek Lim 임성택 Sanofi

Councilor - Outreach Yun H. Choe 최윤 Lucas & Mercanti

Councilor – Chair, Advisory Committee Jae Uk Jeong 정재욱 GSK

Advisory Committee Past KASBP Presidents



2019 KASBP Fall Symposium Committee

Symposium Committee Chair Members

Program Committee Hyun-Hee Lee Wooseok Han, Jae Uk Jeong,

Sung-Kwon Kim

Registration Committee Sungki Kim

Hyelim Kim, Sangwoo Lee,

Sehyin Park, Suhyun Lee, Jihyun

Kim

Fellowship Committee Hakryul Jo / Jennie Jung Mooje Sung, Hyun-Hee Lee

Job Fair Committee Dooyoung Lee Byunheon Choi, Jungmin Park,

Juhee Kim, Hyoyeon Jeong

Networking Committee Sandy Suh Hyeyeong Jang, Juhyun Kim,

Dongeun Kim, Dayun Choi

Finance Committee Sahee Kim Yun H. Choe

PR Committee Kern Hee Chang Hyunjin (Gene) Shin

Graphic Design Jamie Jiyoung Park

On-line Registration and Web

Master Daeho Lee



Symposium Schedule Summary

November 1 (Friday) November 2 (Saturday)

AM 7 7:30 – 8:30 AM Registration and

Breakfast

8:30 – 8:40 AM Opening Remarks

8

8:40 – 11:00 AM Scientific Session

A 9

10

11 11:00 – 11:30 AM Sponsor

Presentation

YG Keynote session

11:30 – 12:30 PM Fellowship

Awards Ceremony PM 12

12:30 – 12:40 PM Group Photo

12:40 – 2:10 PM Lunch and Poster

Session 1 1:00-4:00 PM

KHIDI Forum

(Registration required) 2 2:10 – 4:30 PM Scientific Session

B 3 3:00-6:30

PM

Job Fair

4 4:30 – 4:50 PM Sponsor

Presentation

4:50 – 5:00 PM Closing Remarks

5 5:00 – 5:30 PM Break

5:30 – 6:30 PM Registration

and Networking

5:30 – 7:30 PM

Dinner & Special Session

(registeration required) 6

6:30 – 7:15 PM

Opening & Congratulatory Remarks and

Dinner

7 7:15-7:30 PM

Sponsor Presentation

7:30 -8:00 PM Dinner 7:30 – 7:40 PM

Symposium Closing Remarks

8 7:45-8:45 PM

Award Ceremony

& Keynote Presentation

9 9:15 – 10:40 PM

Industry-Pharma Networking Session

YG Networking/Mentor-Mentee Session 10



Symposium Schedule in Detail

November 1, 2019, Friday

KHIDI Forum (invited speakers and discussion panel: general members participate as observers)

1:00 pm ~ 4:00 pm Organizer: KHIDI & KASBP – K. Stephen Suh, Soo-Hee Park, Wooseok Han

Job Fair (Details will be available at www.kasbp.org)

3:00 pm ~ 5:30 pm Organizer: Dooyoung Lee

Registration & Networking

5:30 pm ~ 6:30 pm Registration Team

Opening & Congratulatory Remarks and Dinner

6:30 pm ~ 7:15 pm Moderator: KASBP President Designated - Soo-Hee Park, Novartis

• Opening Remark KASBP President, K. Stephen Suh, DiagnoCine

• Congratulatory Remarks KPBMA President, Hee-Mok Won

Daewoong CEO & President, Sengho Jeon

Invited Presentation Cooperation of KASBP and KPBMA, Moderator: Soo-Hee Park, Novartis

7:15pm ~ 7:30 pm Korea Pharmaceutical and Bio-Pharma Manufacturers Association

Kyung Hwa Huh

• Prosperity Toast & Dinner Leaders of KRIBB – Hong-Won Lee

Ulsan University – Ja Rok Koo

Award Ceremony KASBP-Daewoong Achievement Award

Moderator: Vice President I - Wooseok Han, Novartis

8:00 pm ~ 8:15 pm Kwang-Soo Kim, Director of Molecular Neurobiology Laboratory at McLean Hospital

and Professor of Psychiatry at Harvard Medial School

Keynote Lecture

8:15 pm ~ 8:45 pm Novel therapeutic development for Parkinson’s disease

Kwang-Soo Kim, Harvard Medical School

Sponsor Presentation Moderator: Wooseok Han, Novartis

8:45 pm ~ 9:15 pm Daewoong Pharmaceuticals

Industry-Pharma Networking Session Moderator: KASBP Member Networking Director - Sandy Suh, Exeltis

9:15 pm ~ 9:20 pm Introduction of Mentor-Mentee Program

KASBP YG Director, Ji Eun Lee, MCPHS

9:20 pm ~ 10:40 pm Members Networking and YG Session

Groups – (1) Computational biology/ data science/ machine learning/ AI, (2) BD/Legal/VC,

(3) Chemistry, (4) Pharmacy, (5) Respiratory/ metabolic/ cardiovascular/ aging/ mental/

neurogenerative, (6) PK/ PD/ pre-clinical/ clinical science, (7) Immuno-oncology/ autoimmune/

inflammatory, (8) Cell and gene therapy/ viral infection/ rare disease



November 2, 2019, Saturday

Registration & Breakfast

7:30 am ~ 8:30 am

Opening Remarks

8:30 am ~ 8:40 am Moderator: Vice President II - Hyun-Hee Lee

Scientific Session A

8:40 am ~ 11:00 am Session Chair: Connecticut Chapter President - Sung-Kwon Kim, Alexion

• A-1: Discovery of E7766: A representative of a novel class of macrocycle-bridged STING agonists

(MBSAs) with pan-genotypic activity.

Daeshik Kim (Eisai)

• A-2: Drug Discovery and Development in Idiopathic Pulmonary Fibrosis.

Sunhwa Kim (Merck)

Coffee Break 10:00 am ~ 10:20 am

• A-3: Strategies to tackle Emerging and Re-Emerging Infectious Diseases.

Ji-Young Min (GSK)

Sponsor presentation: Moderator: KASBP Executive Director - Hanjo Lim, Genentech

11:00 am ~ 11:30 am

• LG Chem Overview of LG Chem Life Sciences R&D

Peter S. Hong, VP, Head of Research

• Samsung BioLogics: Introduction of Samsung BioLogics

Eun Young Yang, Head of CDO Business Team

• KRIBB: Introduction to KRIBB

Yong Hwan Shin, Chief Associate Manager, Policy and Strategy Dept

YG – Keynote Session Moderator: KASBP YG Director – Jieun Lee

11:00 am ~ 12:30 pm Keynote Speakers: Sandy Suh, Richard Oh, Yoomin Chung

Fellowship Award Ceremony Moderator: KASBP Science Director - Hakryul Jo, Agios

Support, Jennie Jung, Sanofi

11:30 am ~ 12:30 pm

Photo time

12:30 pm ~ 12:40 pm

Lunch & Poster Presentation

12:40 pm ~ 2:10 pm

Scientific Session B



2:10 pm ~ 4:30 pm Session Chair: KASBP Washington DC Chapter President - Nam Cheol Kim,

United States Pharmacopeia

• B-1: The present and future of Data Science, Machine Learning and Artificial Intelligence in Drug Discovery

and Development

Hyun-Jin Shin (Takeda)

• B-2: Machine Learning to facilitate understanding of Disease Biology and Drug Discovery

Jang-Hee Woo (Novartis)

Coffee Break 3:30 pm ~ 3:50 pm

• B-3: Gene therapy in the Eye

Jenny JY Song (pH Pharma)

Sponsor Presentation Moderator: KASBP Illinois Chapter President - Seungwon Chung, Abbvie

4:30 pm ~ 4:50 pm

• Ulsan University Ja Rok Koo, Professor

• Celerion Kaz Aoyagi, Senior Director, Business Development

Scientific Session Closing Remarks

4:50 pm ~ 5:00 pm KASBP President - K. Stephen Suh, DiagnoCine

Break

5:00 pm ~ 5:30 pm

Special Session & Dinner: Scientific presentation from KASBP sponsors

Moderator: KASBP Public Relations Director - Kern Chang, Janssen

5:30 pm ~ 7:30 pm

• Samsung BioLogics: Faster & Better, Your Success to IND and BLA, Eun Young Yang, Head of CDO

Business Team

• KRIBB : KRIBB technology: plugging in to regional and global company, Hyung cheol

Kim, Technology Transfer Center

• Celerion : Celerion perspective on IND submissions, Heimo Scheer, VP of Regulatory Affairs

Symposium Closing Remarks

7:30 pm ~ 7:40 pm KASBP President - K. Stephen Suh, DiagnoCine



KEYNOTE LECTURE

BIO & ABSTRACT

Novel therapeutic development for Parkinson’s disease

Kwang-Soo Kim, Harvard Medical School

Biography Dr. Kim’s research has been focused on the transcriptional regulatory cascade of midbrain dopamine neuronal system in health and disease. Based on these studies, Dr. Kim’s recent research is focused on identification and validation of potential drug targets for novel mechanism-based disease-modifying therapeutics development for PD. In addition, Dr. Kim’s lab is investigating molecular mechanisms of somatic reprogramming and in vitro differentiation of hiPSCs for establishing personalized cell therapy of PD. Dr. Kim has published >160 peer-reviewed papers and has trained >100 students, postdocs, and visiting scholars, many of whom are currently working in major universities and institutes in USA, Europe, and Korea. Abstract Based on our studies of transcriptional mechanisms underlying development and maintenance of midbrain dopaminergic neurons, we identified the orphan nuclear receptor Nurr1 as a promising therapeutic target of PD. Although Nurr1 is generally considered to be a ligand-independent constitutively active transcription factor, our data show that Nurr1’s function can be prominently regulated by small molecule agonists/ligands, suggesting that Nurr1’s native and/or synthetic ligands can be developed as a novel class of mechanism-based, disease-modifying therapeutics for PD via direct binding and activation of Nurr1. In addition, given that major motor dysfunction of PD is caused by selective degeneration of midbrain dopamine neurons, cell replacement is a promising approach for PD. Thus, we are developing and optimizing human iPSC-based transplantation for autologous, personalized cell therapy. I will discuss our progress on these translational researches towards novel therapeutic development for PD.



SCIENTIFIC SESSION

SPEAKERS BIO & ABSTRACTS

SESSION A

A-1: Discovery of E7766: A representative of a novel class of macrocycle-bridged STING agonists (MBSAs) with

pan-genotypic activity

Dae-Shik Kim, Eisai

Biography Dae-Shik Kim, Ph.D. is currently a Principal Scientist of Eisai Inc., a global pharmaceutical company with its focus on oncology and neurology. He obtained his B.S. and M.S. degrees in South Korea from Seoul National University and his doctoral degree in 2007 from University of Pennsylvania while working on his research projects under Professor Amos B Smith, III. He joined Professor Kishi’s lab at Harvard University for his postdoctoral training, where he investigated new synthetic routes for Halichondrin. He then joined Eisai in 2009 as a scientist in chemistry. Since then, he has been involved in various projects including process research for BACE inhibitor, development new synthetic routes for Halaven, building macrocycle library, discovery of novel Sting agonist in immuno-oncology, and antisense oligonucleotide. Abstract STING (stimulator of interferon genes) is an emerging target for cancer immunotherapy. 2’,3'-cGAMP, a natural cyclic dinucleotide (CDN) STING agonist, and its phosphorothioate analogs, have drawn broad attention as lead molecules for STING targeted drug discovery. These CDNs, however, lack efficacy in some common STING genotypes disproportionally represented in non-Caucasians. Moreover, such CDNs have not fully addressed liability in chemical/metabolic stability. Here we report our chemistry approach to control STING agonist conformation to enhance binding affinity across all common STING genotypes and broaden the therapeutic potential of such compounds. Our SBDD approach started with analysis of the binding pocket and key protein-ligand interactions to prioritize a focused set of analogs for chemical synthesis. Systematic SAR was built upon in vitro assays for STING binding affinity and activation of STING genotypes. X-ray single crystal structures were established for STING and diverse analogs, in free and bound states, to provide structural insight for rational analog design. Structural modeling was refined to evaluate different binding modes and dynamic conformational changes in the STING-ligand interface. We observed that STING-bound CDNs had the two ancillary nucleobases specifically oriented in close proximity with parallel pi-pi stacking and discovered that covalently linking the nucleobases advantageously pre-organize the bioactive constrained conformation for enhanced STING affinity. Our discovery established a novel class of macrocycle-bridged STING agonists (MBSAs). E7766, a representative of Eisai MBSA platform, shows superior in vitro activity against all the major human STING genotypes over reference CDNs, most distinctly in STINGREF. E7766 co-crystal structures with STINGWT and STINGREF provide structural basis for the added benefit of the topological novelty. The macrocyclic linker bridging the top of nucleobases perturbs the STING lid loop conformation and create new and specific interactions with both genotypes. In twelve subcutaneous tumor models in immune competent mice, single intra-tumoral injections achieved either complete regression or significant tumor growth delay with no serious adverse effect. E7766 also shows excellent chemical and metabolic stability, presumably conferred by conformational rigidity of the unique macrocycle bridge. Eisai successfully discovered E7766, a representative of a novel class of macrocycle-bridged STING agonist topologically distinct from conventional STING agonists. E7766 demonstrated pan-genotypic STING activation, potent anti-cancer activities and excellent chemical and metabolic stability for further development.



A-2: Drug discovery and development in IPF

Sunhwa Kim, Merck & Co., Inc.

Biography Sunhwa Kim, Ph.D. is a principal scientist at Merck Research Laboratory, Merck & Co at South San Francisco with its focus on the pathologic aspects of inflammation and fibrosis in NASH and IPF. Sunhwa obtained her B.S. degree in Microbiology from Kyung-Pook National University in Daegu, Korea and M.S. degree in Microbiology from the University of Tokyo, Japan. Sunhwa obtained her doctoral degree in Immunology at the University of Tokyo as well while working on her research projects under Drs. Taniguchi Tadatsugu and Takayanagi Hiroshi. Sunhwa joined Drs. Anjana Rao lab at the Harvard Medical School in 2004 and Michael Karin lab at the University of California, San Diego in 2005 for her postdoctoral trainings where she investigated epigenetic regulations in T cells and the pathologic roles of inflammation and immunology in tumor progression and metastasis. Sunhwa was the recipient of Human Frontier Scientific program, NCI cancer therapeutics training program, and NIH/NCI F32-NRSA fellowship during her trainings. Sunhwa is an author of >20 of peer-reviewed publications in high impact journals such as Nature, Science, and Developmental Cell. In past over 10 years, Sunhwa has investigated her scientific curiosities in dysregulated immunity, inflammation and fibrosis in drug discovery settings at Janssen pharmaceuticals, a part of Johnson and Johnson; InterMune, a part of Roche/ Genentech; Gilead, and now she is working at Merck Research Laboratory. Sunhwa has been playing key roles in different stages in drug discovery and development such as new target identification, validation; hit/lead identification; new indication mapping for drugs in clinic and biomarker identification. Sunhwa was also a part of discovery team for Pirfenidone, the first approved drug in IPF. Abstract Idiopathic pulmonary fibrosis (IPF) is a debilitating and fatal interstitial lung disease. It causes permanent scarring of the lungs, difficulty breathing and decreases the amount of oxygen the lungs can supply to major organs of the body. The median survival after diagnosis is 2-4 years, which is lower than that reported for many common cancers. Extensive preclinical investigation and numerous clinical trials in past several decades have shed light on the IPF disease etiology and pathophysiology. The discouraging clinical outcomes with anti-inflammatory and immunomodulatory agents have shifted the paradigm of IPF disease pathogenesis from active inflammatory condition to primarily fibrotic condition, led by continuous alveolar epithelial cell injury and aberrant wound healing, resulting in excess accumulation of extracellular matrix/ scar. Importantly, two treatments have been approved for the treatment of IPF, i.e., pirfenidone and nintedanib, in several years ago. The real-world data have proven the benefits of pirfenidone and nintedanib in slowing the progression of the diseases by improving the decline in forced volume capacity, measuring the lung function. However, limited benefits were seen in survival, acute exacerbation, pulmonary hypertension, and established/ progress in fibrosis. Here, I will discuss the emerging therapeutic opportunities in IPF by reviewing IPF disease pathogenesis and market landscape.

A-3: Strategies to tackle emerging and re-emerging infectious diseases

Ji-Young Min, GlaxoSmithKline

Biography Ji-Young Min, Ph.D. is currently the Director and the global project head for new vaccines at GSK. She leads cross-functional teams to drive project strategy and collaborate effectively with internal and external stakeholders. Her responsibility includes managing all aspects of vaccine project from research to launch. She obtained her doctorate degree and prost-doctoral training from the University of Texas at Austin while studying on the influenza virus and its mechanism to evade the host anti-viral responses under the direction of Dr. Robert Krug. In 2008, she joined the laboratory led by Dr. Kanta Subbarao at the National Institutes of Health (NIH) and her research interest focused on the generation of live attenuated reassortant influenza vaccine candidates against avian influenza viruses that have pandemic potential and evaluation of these vaccines in preclinical studies and clinical trials. She then joined the Institute Pasteur in Korea (IPK) to head the Respiratory Viruses Research group focusing on the development of novel small molecules with universal antiviral efficacy. Her group have developed cell based phenotypic high-throughput screening assays and broad spectrum of virological tools and techniques are used to dissect the



mechanism of action and to identify the target. In addition, she took a leadership role to coordinate the Asian Influenza Initiative in Southeast Asia, an initiative that drives basic research, antiviral therapy & diagnostic developments, and surveillance through collaboration of excellent scientists outside and within the Institute Pasteur network. She has a proven record for creative research and directing diverse collaborative teams. Managed multiple complex collaborations and provide strategic and technical advice to improve project outcomes. Multi-task oriented with demonstrated abilities to organize, mentor staff, and make prioritization decisions. Her professional interests include understanding the role of antibodies, supporting the development of efficacious vaccines and therapies against infectious, chronic diseases and cancer with a keen interest to establish global portfolio to have timely public-health impact. Abstract Vector-borne diseases are human illnesses caused by viruses, bacteria and parasites that are transmitted by mosquitoes, sandflies, ticks, lice, mites etc. It represents a major public health problem due to globalization and propagation of susceptible vectors worldwide. Of all disease-transmitting insects, the mosquito is the greatest threat, spreading malaria, dengue, yellow fever, chikungunya, Japanese encephalitis, and Zika, which together are responsible for several millions of deaths and hundreds of millions of cases every year. There are no licensed vaccines against most of these viruses, and vaccine development and use has been complicated by the number of different viruses to protect against, by subtype and strain variation, and by the inability to predict when and where outbreaks will occur. A new approach to preventing arboviral diseases is suggested by the observation that arthropod saliva facilitates transmission of pathogens, including leishmania parasites, Borrelia burgdorferi, and some arboviruses. In this talk, we will discuss on the recent advancements in understanding the roles of arthropod saliva in arthropod borne infections and explore the potential modulatory impact of mosquito salivary proteins on alphavirus pathogenesis. In addition, the potential use of mosquito salivary proteins as therapeutic or vaccine targets for controlling mosquito-borne alphavirus diseases is highlighted.

SESSION B

B-1: The present and future of data science, machine learning and artificial intelligence in drug discovery and

development

Hyunjin (Gene) Shin, Takeda Pharmaceuticals

Biography Dr. Hyunjin (Gene) Shin is a principal scientist in the Translational Bioinformatics/Computational Biology Group at Takeda Pharmaceuticals in Cambridge, Massachusetts. Dr. Shin is a genomics expert in many disease areas including oncology. He currently leads a number of preclinical and clinical projects related to biomarker identification and predictive modeling for patient stratification/precision medicine. Recently, he has been working on reverse translational research by applying natural language processing (NLP) and deep learning (DL) to real-world evidence data such as electronic medical record (EMR). As to his education and training background, Dr. Shin received his B.S. in Electrical Engineering at Seoul National University, Korea in 1998. He completed M.S. and Ph.D. in Electrical and Computer Engineering at the University of Texas at Austin with research of biomedical engineering and biomedical informatics in 2001 and 2006, respectively. In 2007, Dr. Shin joined Dr. X. Shirley Liu’s lab in Department of Biostatistics and Computational Biology at Dana-Farber Cancer Institute/Harvard School of Public Health in Boston, Massachusetts as a postdoctoral research fellow. The main research topics of the time period were the revelation of epigenetic and transcriptional regulatory mechanisms in carcinogenesis and cell development by analyzing next-generation sequencing data such as ChIP-Seq and RNASeq. After his postdoctoral training, he joined Takeda Pharmaceuticals in 2011, and since then he has been working as a leading computational biologist and data scientist at the organization, supporting many translational research projects. Abstract Data science, machine learning, and artificial intelligence have recently attracted attention of the pharmaceutical science community due to their potential to extract information of high utility from notoriously complex biomedical and chemical data. However, we have yet heard many success stories of such new technologies that can make real



contributions to more effective therapeutic development. In my presentation, I will help the audience better understand the basic concepts of machine learning, particularly deep learning based artificial intelligence. Then, I will introduce the current progress being made by those revolutionary methods in the pharmaceutical and biomedical sectors. Finally, I will discuss how we are able to proactively as well as practically prepare for the future of drug discovery and development using these powerful data science tools.

B-2: Clinical Perspectives of Acute Myeloid Leukemia (AML) and The Application of Machine Learning in AML

Therapy

Janghee Woo, Novartis

Biography Dr. Janghee Woo is a clinical program leader at Novartis Institute for BioMedical Research, and clinical assistant professor at Robert Wood Johnson Medical School and Rutgers Cancer Institute of New Jersey. He recently moved from Fred Hutchinson Cancer Research Center (FHCRC) and University of Washington (UW), where he was an attending physician in hematologic malignancy clinic and blood/marrow transplant center. He obtained Ph.D. at Harvard University in 2011 after having received an MD degree at Seoul National University in 2004. After completing Ph.D. training in developmental biology and genetics under the mentorship of Drs. Gary Gilliland and Ramesh Shivdasani, he completed a residency in Internal Medicine at Albert Einstein Medical Center in 2014, followed by Hematology/Oncology fellowship at FHCRC/UW in 2016. His research focused on improving molecular understanding of hematologic malignancy, in particular, myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). He is currently leading malignant hematology programs in early development at Novartis. He was an NCI Paul Calabresi Scholar and a CTI Endowed Fellow at FHCRC and a recipient of the Celgene Hematology Award. Abstract Cancers are genetically heterogeneous diseases in which mapping of clinical behavior is imperfectly aligned with specific mutations. Advances in bioinformatics and computing power provide new opportunities to characterize such features and thus identify higher-risk patients. I will discuss new employment of machine learning in mutation analysis, unsupervised learning in whole-genome or -exome sequencing data from patients with acute myeloid leukemia (AML). This approach allowed us to identify a subset of high-risk patients more likely to fail to respond to induction chemotherapy and have more reduced survival. Feature selection via supervised learning discovered critical mutations differentiating the risk groups and to develop a clinically applicable algorithm to identify high-risk patients. I will further discuss molecular pathways deregulated in the high-risk group of patients and the potential benefits and rationale of combined therapy with novel targeted agents. This approach taking advantage of machine learning could improve clinical outcomes in patients with intermediate-risk AML by avoiding sole use of conventional induction chemotherapy in patients with a high risk of response failure.

B-3: Gene Therapy in The Eye

Jenny JiYun Song, pH Pharma

Biography Jenny JiYun Song, Ph.D. is currently the Preclinical Ophthalmology Lead in pH-Pharma, Co., Ltd., a biotechnology company with its focus on Glaucoma, NASH and ADC. She obtained her doctoral degree from KAIST while working on her research projects under Dr. Dae-Sik Lim. She was the recipient of Overseas Research Support for the Next Generation Scientists fellowship and Overseas Training Program fellowship during her training. She joined Dr. Jean Bennett’s lab at the University of Pennsylvania] for her postdoctoral training in ophthalmology gene therapy, where she investigated proof-of-concept study for LCA5, an early onset congenital disease due to a Lebercilin gene defect. She played a leading role in developing rAAV-mediated LCA5 gene therapy drug into clinical stages, which led to the successful establishment of a partnership with Foundation Fighting Blindness. She then joined Spark Therapeutics in 2017 as a preclinical scientist working on new programs as well as post-approval drug, Luxturna, the first gene therapy drug approved by FDA. She recently joined to pH-Pharma as an ophthalmology lead to establish new ophthalmology programs including gene therapy program and to manage non-clinical studies. She serves as a



product development consultant of the PEX1 gene therapy project for the teams in McGill University who has the support from AmorChem and GFPD. Abstract Ever since rAAV-mediated gene therapeutic approach opened a door to the patients who used to have no cure for their inherited visual disorders, laboratory-based gene therapy technology has evolved continuously. This emerged to clinical application and expanded its application to variety of fields including CAR T-cell therapy. Here we revisit the history of retinal gene therapy with the story of Leber’s Congenital Amaurosis and discuss considerations for gene therapy product development. Recently, innovative new drugs from gene and cell therapy area have reported significant progress in their clinical trials for the treatment of AMD, a complex degenerative ophthalmic disease with unmet medical needs. The lessons learned from safety and efficacy trials support a path forward aiming to further trials and finally a new drug registration in the near future.

SATURDAY DINNER & PANEL DISCUSSION

"Scientific presentation from KASBP sponsors"

• Samsung BioLogics : Faster & Better, Your Success to IND and BLA, Eun Young Yang, Head of CDO Business Team

• KRIBB: KRIBB technology: plugging in to regional and global company,

Hyung cheol Kim, Technology Transfer Center

• Celerion: Celerion perspective on IND submissions, Dr. Heimo Scheer



POSTER SESSION

AWARDEE ABSTRACTS

2019 FALL FELLOWSHIP AWARDEES

AWARD NAME AWARDEE AFFILIATION

KASBP–Daewoong Fellowship Hyunyong Koh, Ph.D Boston Children’s Hospital

KASBP–Daewoong Fellowship Young Cha, Ph.D McLean Hospital

KASBP–Daewoong Fellowship Hojong Yoon, Ph.D Student

Harvard University

KASBP-LG Chem Fellowship Jea Hyun Baek, Ph.D Biogen Inc.

KASBP-LG Chem Fellowship Donggi Paik, Ph.D Harvard Medical School

KASBP-Samsung Biologics

Fellowship

Eunju Im, Ph.D Nathan S. Kline Institute for Psychiatry Research

KASBP-Samsung Biologics

Fellowship

Jongho Park, Ph.D Massachusetts General Hospital

KASBP-KRIBB Fellowship Soohong Min, Ph.D Harvard Medical School

KASBP-KRIBB Fellowship Eun-Ik Koh, Ph.D University of Massachusetts Medical School

KASBP Fellowship Kyusik Kim, Ph.D Student

University of Massachusetts Medical School

P-1: BRAF somatic mutation contributes to intrinsic epileptogenicity in pediatric brain tumors

Hyunyong Koh, Ph.D

Boston Children’s Hospital

Pediatric brain tumors are highly associated with epileptic seizures. However, the epileptogenic mechanisms in epilepsy-associated tumors remain unclear. Here, we show that the oncogenic BRAF somatic mutation p.Val600Glu (V600E) in developing neurons underlies intrinsic epileptogenicity in ganglioglioma (GG), one of the leading causes of pediatric intractable epilepsy. To do so, we developed a mouse model harboring the BRAF V600E somatic mutation during early brain development to reflect the most frequent mutation, as well as the origin and timing thereof, in GG. Therein, we noted that BRAF V600E mutation arising in early progenitor cells during embryonic brain development led to the acquisition of intrinsic epileptogenic properties in neuronal lineage cells, whereas tumorigenic properties were attributed to high proliferation of glial lineage cells exhibiting the mutation. RNA-seq analysis of patient brain tissues with the mutation further revealed that BRAF V600E-induced epileptogenesis is mediated by RE1-Silencing Transcription Factor (REST), a regulator of ion channels and neurotransmitter receptors associated with epilepsy. Moreover, we found that seizures in mice were significantly alleviated by an FDA-approved BRAF V600E inhibitor, Vemurafenib, as well as various genetic inhibitions of REST activity. Accordingly, this study provides direct evidence of a BRAF somatic mutation contributing to the intrinsic epileptogenicity in pediatric brain tumors and suggests that BRAF and REST could be treatment targets for intractable epilepsy.

P-2: Functional roles of Sirtuins as metabolic regulator controlling human pluripotent stem cell fate

Young Cha, Ph.D

McLean Hospital

Metabolic reprogramming from mitochondrial oxidative phosphorylation (OXPHOS) toward glycolysis is critical for somatic cell reprogramming of induced pluripotent stem cells (iPSCs). Although this metabolic reprogramming



appears to be a fundamental aspect of human induced pluripotency and stem cell fate control, the molecular mechanisms underlying the link between energy metabolism and stem cell fate are poorly understood. Here, we found that protein acetylation is a fundamental aspect of stem cell fate control and critically regulate induced pluripotency and metabolic reprogramming. In particular, we report that SIRT1 upregulation and SIRT2 downregulation is a molecular signature of human pluripotent stem cells. In addition, we investigated specific roles that are coordinated by SIRT1 and other sirtuins and their potential downstream targets and regulatory mechanisms underlying metabolic reprogramming. Furthermore, we explored how various microRNAs can regulate sirtuins, leading to metabolic reprogramming and control pluripotent stem cell fate and function. We will discuss our findings regarding potential functional roles of sirtuins and microRNAs as modulators of metabolic reprogramming during human induced pluripotency and pluripotent stem cell function.

P-3: Structural complementarity facilitates E7820-mediated degradation of RBM39 by CRL4DCAF15

Hojong Yoon, Ph.D

Harvard University

The investigational drugs E7820, indisulam and tasisulam (aryl-sulfonamides) promote the degradation of the splicing factor RBM39 in a proteasome and CRL4DCAF15 ubiquitin ligase-dependent mechanism, however the molecular details of this activity remain elusive. Here we present the cryo-EM structure of DDB1-DCAF15-DDA1 bound to RBM39 and E7820 at 4.4 Å resolution, together with crystal structures of engineered subcomplexes. We show that DCAF15 adopts a novel fold stabilized by DDA1, and that extensive protein-protein contacts between the ligase and substrate mitigate the low affinity interaction between aryl-sulfonamides and DCAF15. Our data demonstrates how aryl-sulfonamides neo-functionalize a shallow, non-conserved pocket on DCAF15 to selectively bind and degrade RBM39 and RBM23 without the requirement for a high affinity ligand, which has broad implications for the de novo discovery of molecular glue degraders. P-4: Dimethyl Itaconate Suppresses TLR-mediated Early Inflammatory Response

Jea Hyun Baek, Ph.D

Biogen Inc.

Itaconate is intracellularly derived from cis-aconitate, an intermediate in the tricarboxylic acid (TCA) cycle, and is accumulated in activated immune cells (e.g., macrophages) in response to immune activation. Itaconate has recently emerged as an immunomodulatory molecule with high therapeutic potential. However, since the native form of itaconate is cell-impermeable, it is necessary to develop a derivate of itaconate with increased intracellular penetrance without impairing immunosuppressive properties of the native molecule. In particular, dimethyl itaconate (DMI), the methyl ester of itaconic acid, is highlighted as a promising therapeutic. DMI shows a highly electrophilicity, similar to the structurally related dimethyl fumarate (DMF), a leading therapy in psoriasis and multiple sclerosis. In this study, we sought to compare the targets of DMI versus DMF using a proteomic cysteine-reactivity profiling in non-immune cells and analyze the impact of DMI on immune signaling pathways. Especially, we were interested in investigating whether DMI and DMF target the glycolytic metabolism in non-immune cells as DMF was reported to bind to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in activated macrophages. In our study, we found that DMI and DMF suppress toll-like receptor (TLR) 3-mediated nuclear factor kappa light chain enhancer of activated B cells (NF-B) signaling pathways, not altering immunometabolism. P-5: Bile acid metabolites control Th17 and Treg cell differentiation

Donggi Paik, Ph.D

Harvard Medical School

Bile acids are abundant in the mammalian gut where they undergo bacteria-mediated transformation, generating a large pool of bioactive molecules. Although bile acids are known to affect host metabolism, cancer progression and innate immunity, it is unknown whether they affect adaptive immune cells such as T helper cells expressing IL-17a (Th17 cells) and regulatory T cells (Tregs). By screening a library of bile acid metabolites, we identified two distinct derivatives of lithocholic acid (LCA), 3-oxoLCA and isoalloLCA, as T cell regulators. 3-oxoLCA inhibited Th17 cell differentiation by directly binding to its key transcription factor RORγt (retinoid-related orphan receptor γt) and



isoalloLCA enhanced Treg differentiation through the production of mitochondrial reactive oxygen species (mitoROS), leading to increased FoxP3 expression. IsoalloLCA-mediated Treg enhancement required an intronic FoxP3 enhancer, the conserved noncoding sequence 3 (CNS3), a distinct mode of action from previously-identified Treg enhancing metabolites that require CNS11,2. Administration of 3-oxoLCA and isoalloLCA to mice reduced Th17 and increased Treg cell differentiation in the intestinal lamina propria. Our data suggest novel mechanisms by which bile acid metabolites control host immune responses by directly modulating the Th17 and Treg balance.

P-6: Fyn kinase Dependent Tyrosine Phosphorylation of APP-βCTF Regulates vATPase-mediated Lysosomal

Acidification

Eunju Im, Ph.D

Nathan S. Kline Institute for Psychiatry Research

Early appearing, progressive lysosomal dysfunction is a prominent pathophysiological feature in Alzheimer’s disease (AD), linked to major causative and risk genes for AD and diverse aspects of AD pathology, including neurodegeneration. Elevation of beta-secretase C-terminal fragment of amyloid precursor protein (APP-βCTF) disrupt lysosomal acidification in Down Syndrome (DS) is relevant to sporadic AD. Here, we investigated how APP influences lysosomal function and the underlying mechanism(s) in lysosomes from human DS fibroblasts and DS mouse brain as well as early-onset AD mouse model. In control, APP-βCTF traffics to lysosomes where it interacts selectively with specific subunits of the lysosomal vATPase complex controlling association of the V0/V1 sectors of the complex which regulates activity and luminal acidification. At elevated levels, APP-βCTF competes with these subunits for complex assembly, lowering their levels on lysosomes and promoting dissociation of the V0/V1 sectors, which results in pH elevation. It is controlled by Fyn kinase dependent tyrosine phosphorylation of APP-βCTF. Multiple distinct effects of aberrant APP-βCTF signaling on endosomal-lysosomal function are likely primary contributors to AD pathogenesis, underscoring the close relationship between the major AD-related genes and early endosomal-lysosomal pathway dysfunction.

P-7: IL-33 nuclear regulation promotes immunosuppressive function for cancer development in chronic

inflammation

Jongho Park, Ph.D

Massachusetts General Hospital

Interleukin (IL)-33 is a member of the IL-1 family of cytokines that promotes Th2 response in lymphocytes and activates both mast cells and eosinophils via its receptor, Interleukin 1 receptor-like 1 (IL1RL1 or ST2). Although the participation of IL-33 in chronic inflammatory and autoimmune diseases has become increasingly evident, the source of IL-33 remains elusive. In contrast to other members of this cytokine family, IL-33 is mainly produced by epithelial cells and fibroblasts. Interestingly, IL-33 has a Nuclear Localization Sequence (NLS), and it is localized in the nucleus of epithelial cells during steady state condition. In addition, IL-33 has been shown to act as a transcriptional repressor. However, the collective impact of IL-33, as a cytokine and a nuclear factor, on cancer remains uncertain. Herein, we demonstrate that IL-33 is highly expressed in the nucleus of skin keratinocytes and pancreas epithelial cells in chronic inflammation and induces cancer development in these organs. We found that nuclear function of IL-33 was responsible for the tumor promoting impact of IL-33, which related to its direct regulation of TGF-β signaling, that drive a severe immunosuppression in the epithelial cells. Considering that IL-33 is highly expressed in epithelial cancer cells and their perilesional tissues in humans, our findings highlight the importance of blocking IL-33 expression instead of its cytokine function alone and will have a direct impact on cancer immunotherapy, especially in cancers associated with an immunosuppressed “cold” microenvironment. P-8: Arterial baroreceptors sense blood pressure through decorated aortic claws Soohong Min, Ph.D


Mechanosensory neurons across physiological systems sense force using diverse terminal morphologies. Arterial baroreceptors are sensory neurons that monitor blood pressure for real-time stabilization of cardiovascular output.



Various aortic sensory terminals have been described, but those that sense blood pressure are unclear due to a lack of selective genetic tools. Here, we find that all baroreceptor neurons are marked in Piezo2-ires-Cre mice, and then use genetic approaches to visualize the architecture of mechanosensory endings. Cre-guided ablation of vagal and glossopharyngeal PIEZO2 neurons eliminates the baroreceptor reflex, and aortic depressor nerve effects on blood pressure and heart rate. Genetic mapping reveals that PIEZO2 neurons form a distinctive mechanosensory structure: macroscopic claws that surround the aortic arch and exude fine end-net endings. Other arterial sensory neurons that form flower spray terminals are dispensable for baroreception. Together, these findings provide structural insights into how blood pressure is sensed in the aortic vessel wall.

P-9: Chemical-genetic interactions of essential Mycobacterium tuberculosis systems

Eun-Ik Koh, Ph.D


Tuberculosis (TB) is one of the most prevalent infectious diseases in human history. Approximately a third of the world’s population has been exposed to Mycobacterium tuberculosis (Mtb), the causative agent of TB, with more than 1 million deaths annually. TB must be treated with combinations of antibiotics to minimize the emergence of resistance but despite this complex regimen, TB cure requires months of therapy and multiple drug resistant (MDR) strains continue to emerge. Therefore new strategies are needed to both accelerate cure and treat MDR infections. The requirement for multi-drug therapy represents both a limitation and an opportunity. While combining agents can dramatically increase efficacy, predicting which potential new drugs will produce a synergistic effect in the relevant environmental conditions remains a challenge. Here we utilize conditional Mtb mutants of essential genes to investigate antibiotic-genetic interactions that occur during infection and compare with relevant in vitro conditions such as different carbon sources. Mice were infected with pooled libraries of conditional mutants and subsequently treated with different antibiotics. Novel synergistic interactions were identified compared to untreated controls with hypomorphs of genes associated with multiple pathways including cell wall biosynthesis, metabolism and translation. Synergies found in vivo were also identified in vitro in both carbon source independent and dependent manner, with specific synergies found during cholesterol and fatty acid growth conditions. As the availability of different carbon sources dramatically influences Mtb metabolism and physiology, synergies observed in specific carbon sources may suggest novel metabolic roles for corresponding genes and pathways. Furthermore, synergies with mutants associated with essential amino acid biosynthesis pathways were reversed upon supplementation with corresponding metabolites, suggesting depletion of specific amino acid pools alters the efficacy of antibiotics. By creating an atlas of chemical-genetic interactions of essential genes in different in vivo and in vitro conditions, we can identify new synergies that can be exploited for drug development as well as predict conditions that reflect different infection environments.

P-10: Cyclophilin A protects HIV-1 from restriction by human TRIM5α

Kyusik Kim, Ph.D Student


The abundant cellular protein Cyclophilin A (CypA) was found to bind to HIV-1 capsid (CA) in 1993. Disruption of the CA−CypA interaction decreases HIV-1 infectivity in human cells but stimulates infectivity in non-human primate cells. Genetic and biochemical data suggest that CypA protects HIV-1 from a CA-specific restriction factor in human cells. Discovery of the CA-specific restriction factor tripartite-containing motif 5α (TRIM5α) and multiple, independently derived, TRIM5−CypA fusion genes pointed to human TRIM5α being the CypA-sensitive restriction factor. However, using human cancer cell lines, attempts to obtain evidence that CypA inhibits HIV-1 restriction by the human TRIM5α, let alone that human TRIM5α restricts HIV-1, were unsuccessful. We decided to revisit the question of the mechanism by which CypA increases HIV-1 infectivity by exploiting lentiviral vectors optimized for primary human blood cells. We have now confirmed that disruption of the CA-CypA interaction decreases HIV-1 infectivity in primary human blood cells. The HIV-1 infectivity recovered when TRIM5α was knocked down. Rescue of the TRIM5α knockdown by expression of a non-targetable, human TRIM5α cDNA restored the restriction activity. Furthermore, endogenous TRIM5α associated with virion cores as they entered the cytoplasm, but only when the CA−CypA interaction was disrupted. These experiments resolve the long-standing mystery of the



role of CypA in HIV-1 replication by demonstrating that this ubiquitous cellular protein shields HIV-1 from previously inapparent restriction by human TRIM5α. These results also indicate that non-immunosuppressive CypA inhibitors have the potential to make an important contribution to anti-HIV-1 drug cocktails, by rendering HIV-1 susceptible to the potent antiviral activity of TRIM5α. P-11 Mechanisms underlying synergy of DNA Topoisomerase I and mTOR kinase co-inhibition in malignant

peripheral nerve sheath tumors (MPNSTs)

Dong Hyuk Ki, Ph.D

Dana-Farber Cancer Institute

Background: Malignant peripheral nerve sheath tumors (MPNSTs) are very aggressive and metastatic soft tissue sarcomas. MPNSTs frequently arise in patients with neurofibromatosis type 1 (NF1) which is caused by mutations in the NF1 gene. Since NF1 contains a small region of homology to the Ras GAP protein, NF1-loss results in aberrant activation of Ras signaling and predisposes NF1 patients to a variety of cancers, including MPNSTs. Most of MPNSTs are unresectable at diagnosis and minimally responsive to conventional treatment. Therefore, identification of new genetic dependencies and drugs with anti-tumor activity will be critical to advance MPNST therapy. Methods: To identify effective compounds, we examined a series of candidate agents for their ability to induce apoptosis in MPNST cells arising in nf1/tp53-deficient zebrafish. The compounds showing drug response in the embryonic implantation assay were evaluated by various experimental methods in human NF1-associated and sporadic MPNST cell lines. Results: After testing a series of drugs, we found that DNA topoisomerase I-targeted drugs and mTOR kinase inhibitors were the most effective single agents in eliminating MPNST cells without prohibitive toxicity. In addition, three members of these classes of drugs, either AZD2014 or INK128 in combination with irinotecan, acted synergistically to induce apoptosis both in vitro and in vivo. In mechanistic studies, irinotecan not only induces apoptosis by eliciting a DNA damage response, but also acts synergistically with AZD2014 to potentiate the hypophosphorylation of 4E-BP1, a downstream target of mTORC1. Profound hypophosphorylation of 4E-BP1 induced by this drug combination causes an arrest of protein synthesis, which potently induces tumor cell apoptosis. Depletion of 4E-BP1 in NF1-associated MPNST cells abolished the synergy between DNA topoisomerase I-targeted drugs and mTOR kinase inhibitors in killing MPNST cells, establishing cooperative effects driving 4E-BP1 hypophosphorylation as the mechanism of synergy. Conclusions: The synergy between DNA topoisomerase I-targeted drugs and mTOR kinase inhibitors in our MPNST model appears to be mediated through the mTORC1/4E-BP1 signaling pathway, which regulates the translation of cap-dependent RNAs. Our findings provide a compelling rationale for further in vivo evaluation of the combination of DNA topoisomerase I-targeted drugs and mTOR kinase inhibitors against these aggressive nerve sheath tumors.

P-12: Mitochondrial antiviral signaling protein (MAVS)-mediated resistance against apoptotic cell death is crucial

to lung fibrosis in mice

Sang-Hun Kim, Ph.D

Yale school of medicine

Mitochondrial Antiviral Signaling protein (MAVS) functions as a key platform molecule that mediates damage-associated molecular patterns (DAMPs)-induced innate immune responses. DAMPs signaling has been implicated in the pathogenesis of fibrosis, a common pathologic consequence of various chronic disorders such as idiopathic pulmonary fibrosis (IPF). Our understanding of its underlying mechanism, however, remains poor. How MAVS may function to modulate DAMPs signaling and the consequent fibrosis, in particular, has not been explored yet. Here, we demonstrate that MAVS plays a crucial role in the induction of HMGB1, NLRP3 and cGAS-STING pathways, respectively, and the resultant experimental pulmonary fibrosis after bleomycin-induced injury in vivo, a mammalian model of IPF. Notably, multimeric STING aggregation is significantly attenuated via a MAVS-dependent manner. Mechanistic studies using in vivo as well as in vitro studies reveal that MAVS imposes resistance against apoptotic cell death while facilitates necroptotic cell death. Intriguingly, RIP1/RIP3 hetero-amyloid complex is formed via a



MAVS-dependent manner in vivo. In accordance with this, a combined treatment with necroptosis inhibitor (necrostatin-1) and apoptosis inducer (ABT-263), which recapitulates cell death-related molecular events occurring in MAVS deficiency, synergistically ameliorates lung fibrosis in our IPF modeling. Importantly, persistent MAVS aggregation, a key event of MAVS signaling activation, is observed in lungs from the patients with IPF as well as in mice. In conclusion, MAVS may play an important role in the pathogenesis of IPF and targeting MAVS or its signaling may provide a novel therapeutic strategy for IPF, a major unmet medical need. P-13: Muscle cell-autonomous disease-causing effects of low Survival Motor Neuron protein

Jeong-Ki Kim, Ph.D

Columbia University

Paucity of the Survival Motor Neuron (SMN) protein results in the common, frequently fatal infantile-onset motor neuron disorder, spinal muscular atrophy (SMA). Augmenting the protein is being pursued as a means to a treatment for the disease and recently led to FDA approval of an intrathecally delivered SMN-enhancing oligonucleotide currently in use. Notwithstanding the advent of this and other novel therapeutic options for SMA patients, it is unclear whether the paralysis associated with the disease derives solely from dysfunction of motor neurons and can therefore be entirely precluded following restricted restoration of SMN to the nervous system, or stems from broader defects of the motor unit, arguing for systemic repletion of the protein. To investigate the disease-contributing effects of low SMN in one relevant peripheral organ – skeletal muscle – we used model mice to selectively deplete the protein in just this tissue. We show that muscle deprived of SMN is profoundly damaged. While a disease phenotype may not be immediately obvious, persistent low levels of the protein eventually result in muscle fiber defects, neuromuscular junction abnormalities, compromised motor performance and premature death. Importantly, restoring SMN protein levels following the onset of muscle pathology reverses disease. Our results provide the most compelling evidence yet for a direct contributing role of muscle in SMA and argue that an optimal therapy for the disease must be designed to treat this aspect of the dysfunctional motor unit. P-14: SEPHS2 is essential to prevent selenium poisoning during selenocysteine biosynthesis in cancer cells

Namgyu Lee, Ph.D


Metabolic enzymes are recognized for the products they form, but the significance of their roles in removing toxic substrates in cancer cells is unclear. Through a focused genetic screen for enzymes that may play roles in preventing toxic metabolite accumulation, we identified SEPHS2, a step in the pathway that metabolizes selenium to form the amino acid selenocysteine, a required residue in selenoproteins. SEPHS2 is essential to the survival of a subset of cancer cells including breast and glioma cells, but dispensable to a wide panel of nontransformed cells. Surprisingly, selenocysteine production itself is not essential for cell survival - nontransformed cells can tolerate knockout of SEPHS2 indefinitely despite having lost all capacity to produce selenoproteins. However, due to a novel function of the cysteine/glutamate antiporter SLC7A11 in promoting selenium uptake and selenocysteine biosynthesis, many cancer cells are ‘selenophilic’ and are acutely dependent on SEPHS2 to process and thus prevent accumulation of selenide, a toxic intermediate in the pathway. As SEPHS2 is itself a selenoprotein, we find that SEPHS2 expression is induced by excess selenium, thereby matching detoxification capacity to selenium supply. Accordingly, SEPHS2 mRNA and protein levels are elevated in human breast cancer patient samples and disruption of SEPHS2 impairs growth of orthotopic mammary tumor xenografts. Thus, the toxicity of selenium is dependent on its conversion to selenide, and SEPHS2 is a selective therapeutic target to induce poisoning in cancer cells that have an increased appetite for selenium. P-15: Erosion of the Epigenetic Landscape and Loss of Cellular Identity as a Cause of Aging in Mammals

Jae-Hyun Yang, Ph.D


All living things experience entropy, manifested as a loss of inherited genetic and epigenetic information over time. As budding yeast cells age, epigenetic changes result in a loss of cell identity and sterility, both hallmarks of yeast aging. In mammals, epigenetic information is also lost over time, but what causes it to be lost and whether it is a



cause or a consequence of aging is not known. Here we show that the transient induction of genomic instability, in the form of a low number of non-mutagenic DNA breaks, accelerates many of the chromatin and tissue changes seen during aging, including the erosion of the epigenetic landscape, a loss of cellular identity, advancement of the DNA methylation clock and cellular senescence. These data support a model in which a loss of epigenetic information is a cause of aging in mammals. P-16: Global targeting of functional tyrosines using sulfur triazole exchange chemistry

Heung Sik Hahm, Ph.D

University of Virginia

Covalent probes serve as valuable tools for global investigation of protein function and ligand binding capacity. Despite efforts to expand coverage of residues available for chemical proteomics (e.g. cysteine and lysine), a large fraction of the proteome remains inaccessible with current activity-based probes. Here, we introduce sulfur-triazole exchange (SuTEx) chemistry as a tunable platform for developing covalent probes with broad applications for chemical proteomics. We show modifications to the triazole leaving group can furnish sulfonyl probes with ~5-fold enhanced chemoselectivity for tyrosines over other nucleophilic amino acids to investigate, for the first time, more than 10,000 tyrosine sites in lysates and live cells. We discovered tyrosines with enhanced nucleophilicity are enriched in enzymatic, protein-protein interaction, and nucleotide recognition domains. We apply SuTEx as a chemical phosphoproteomics strategy to monitor activation of phosphotyrosine sites. Collectively, we describe SuTEx as a biocompatible chemistry for chemical biology investigations of the human proteome. P-17: Role of the Gut Microbiota in Regulating Responses to anti-PD-1 Cancer Immunotherapy

Joon Seok Park, Ph.D


The human gut is colonized by 100 trillion bacteria collectively referred to as the gut microbiota, which plays an essential role in health and disease. Commensalism in the gut has been suggested to influence many aspects of human health and diseases. It is now widely accepted that gut commensal microbes have a crucial impact on immune homeostasis in the gut. Emerging evidence suggest that the gut microbiota shapes systemic immunity, but the underlying mechanisms are poorly understood. Recent reports from other groups and our preliminary findings indicate that the gut microbiome and its composition are important factors that determine responsiveness to immune checkpoint blockade 1-3. Immune checkpoint inhibitors are novel therapeutic interventions which reinvigorate tumor-specific T cells to attack tumor cells by targeting co-inhibitory pathways in T cells, such as PD-1:PD-L1 and CTLA-4. Despite the clinical success of these checkpoint blockade immunotherapies, a significant fraction of patients do not respond to the checkpoint inhibitors 4. Recent studies showed that one of the critical determinants of responsiveness to checkpoint blockade may be the composition of the gut microbiome. However, how the gut microbiota modulates systemic immune responses to tumor is not known. We aim to determine mechanisms by which the gut microbiome regulates anti-tumor immunity and response to PD-L1 blockade. Using gnotobiotic techniques and antibiotics, we identified human gut microbes that promote tumor clearance upon PD-L1 blocking antibody treatment. Furthermore, colonization of germ-free mice with the healthy human microbiota or our bacterial isolates induces significant changes in the adaptive immune system, suggesting potential cellular and molecular mechanisms of gut microbiota dependent anti-tumor immunity. Finally, we are further investigating the role of microbial products from the gut in regulating anti-tumor immunity. This study provides critical insights into mechanisms by which the gut microbiota regulates anti-tumor immunity, and new therapeutic strategies for patients who do not respond to PD-1 pathway blockade. P-18: Developmental programming of long-term immunity of CD8 T cells by perinatal glucocorticoid

Jun Young Hong, Ph.D

Yale University

Stress has been associated with various types of diseases including cancer. It was suggested that

compromised anti-tumor immunity is often responsible for tumor progression during stress, which is caused by immunosuppressive glucocorticoid (GC), a stress hormone, and sympathetic nervous system activation. Perinatal



period is critical for immunity as the first major contact with the environment is made and this interaction can shape the immune system development. Epidemiologic studies found that early-life exposure to specific environment may have life-long impact on immunity, affecting the development of immune-related diseases such as inflammatory diseases, metabolic diseases, allergic diseases as well as cancer. Nevertheless, it is still largely unknown whether developmental programming of immunity exists due to the lack of mechanistic understanding on this subject.

Since most of the early environmental factors that are reported to cause later-life development of diseases are associated with stress, we adopted a model to directly test the effect of stress hormone. We introduced the in vivo mouse model of perinatal glucocorticoid receptor (GR) activation via dexamethasone (DEX) treatment in drinking water perinatally (embryonic day 7.5-postnatal day 1). Then, we analyzed the T cell immunity when the offspring became mature. We found that perinatal GC exposure elicited diminished CD8 T cell response in adulthood. As a result, mice with perinatal GC treatment showed insufficient anti-tumor and anti-bacterial CD8 T cell responses, being susceptible to immunogenic tumor development and Listeria infection. We found significantly reduced systemic levels of corticosterone (CORT) in the adult mice with perinatal GC exposure. Deficiency of GR signaling in CD8 T cells with adrenalectomy or with genetic deletion of GR in T cells was sufficient to reduce CD8 T cell response. Inhibition of GR signaling in CD8 T cells acted primarily on CD25 signaling and mTOR pathway, resulting in decreased effector function and survival. Finally, we found the negative feedback threshold of HPA axis is altered by having enhanced mineralocorticoid receptor (MR; type I corticosteroid receptor) expression in the hippocampus and paraventricular nucleus of hypothalamus (PVH) with perinatal GC exposure. Our study shows that perinatal stress may have long-term consequences on CD8 T cell immunity by altering HPA axis threshold, thereby increasing predisposition to cancer and bacterial infection.

These results showed that perinatal GC exposure persistently programed the threshold for hypothalamus-pituitary-adrenal axis for regulating endogenous GC level, and that reduced systemic GC level elicited repressed CD8 T cell activation and survival, leading to tumor susceptibility.

P-19: Prioritizing SNP (Single Nucleotide Polymorphism) Set by Joint Model Selection

Juhyun Kim, Ph.D Student

UCLA

Improved personalized treatments are key to improving health care. In spite of dramatic developments in both pharmacogenomic knowledge and the techniques used to perform pharmacogenomic studies, multiple challenges still exist that slow the translation of pharmacogenomic discoveries from "bench to bedside."Variation in response to drug therapies results not only from gene sequence variation, ultimately resulting in differences in mRNA and protein expression, but also other patient characteristics such as clinical and environmental factors. However, few statistical methods exist to maximize use of the extensive genomic data and prior biological knowledge in order to unravel the etiology of complex drug-response phenotypes. We proposed to develop innovative statistical analytical tools and supporting software to integrate prior biological knowledge, such as function or known relationship between genes, with genomic data that will facilitate the generation of novel pharmacogenomic hypotheses. Rare genetic variants are thought to be the key to elucidating the genetic architecture of common diseases and complex traits. Single nucleotide polymorphism (SNP) set analysis aggregates both common and rare variants and tests for association between a phenotype of interest and a set. However, multiple genes, pathways, or sliding windows are usually investigated across the whole genome, in which all groups are tested separately followed by multiple testing adjustment. We propose a minorization-maximization (MM) algorithm that selects relevant variance components to prioritize SNP sets. It is achieved by incorporating penalties, including lasso, adaptive lasso, and minimax concave penalty (MCP). Simulation studies demonstrate the superiority of our methods in model selection performance, compared to the traditional marginal testing methods. We apply our method to a real Merck pharmacogenomics study. P-20: Tissue-restricted Genome Editing in vivo Specified by MicroRNA-repressible Anti-CRISPR Proteins

Jooyoung Lee, Ph.D Student


CRISPR-Cas systems are bacterial adaptive immune pathways that have revolutionized biotechnology and biomedical applications. Despite the potential for human therapeutic development, there are many hurdles that



must be overcome before its use in clinical settings. Some clinical safety concerns arise from editing activity in unintended cell types or tissues upon in vivo delivery [e.g. by adeno-associated virus (AAV) vectors]. Although tissue-specific promoters and serotypes with tissue tropisms can be used, suitably compact promoters are not always available for desired cell types, and AAV tissue tropism specificities are not absolute. To reinforce tissue-specific editing, we exploited anti-CRISPR proteins (Acrs) that have evolved as natural countermeasures against CRISPR immunity. To inhibit Cas9 in all ancillary tissues without compromising editing in the target tissue, we established a flexible platform in which an Acr transgene is repressed by endogenous, tissue-specific microRNAs (miRNAs). We demonstrate that miRNAs regulate the expression of an Acr transgene bearing miRNA-binding sites in its 3’ UTR and control subsequent genome editing outcomes in a cell-type specific manner. We also show that the strategy is applicable to multiple Cas9 orthologs and their respective anti-CRISPRs. Furthermore, we validate this approach in vivo by demonstrating that AAV9 delivery of Nme2Cas9, along with an AcrIIC3Nme construct that is targeted for repression by liver-specific miR-122, allows editing in the liver while repressing editing in an unintended tissue (heart muscle) in adult mice. This strategy provides safeguards against off-tissue genome editing by confining Cas9 activity to selected cell types. P-21: Multiple negative transcriptional regulators can fine-tune actively transcribed genes

Mijeong Kim, Ph.D Student

The University of Texas at Austin

Global gene expression helps determine cellular identity and function. Dysregulation of gene expression contributes to numerous diseases including developmental disorders and cancers; thus, cells must tightly regulate gene expression to maintain homeostasis. Gene regulation occurs at multiple levels, notably via interplay between cis-regulatory elements (such as enhancers and promoters) and trans-acting factors like transcription factors (TFs). In the past, transcriptional regulation was thought of as an “on and off” process in which the binding of repressors to a gene’s regulatory elements was considered evidence of the total suppression of the gene. However, recent groups have observed that highly transcribed genes are occupied by both activators and repressors, leading to a more nuanced view that co-occupancy by both types of regulators allows fine-tuning of gene expression to optimal levels. For example, co-repressors such as histone deacetylases (HDACs) paradoxically occupy many actively transcribed genes in embryonic stem (ES) cells in concert with histone acetyltransferases like p300. Such fine-tuning is necessary, as ES cell core factors like Oct4 must be precisely controlled to maintain cell identity; elevated levels of Oct4 lead to premature loss of stemness in ES. Oct4 and other core factors activate themselves in a positive feedback loop, and a select few repressors like Tgif1 and Tcf3 have been shown to restrain this feedback loop. However, whether other such repressors exist, the molecular and epigenetic mechanisms of these repressors, and their roles in other cell types like cancer cells remain relatively unknown. In this study, we use ES cells as a model system and seek to identify TFs that play a role as transcriptional fine-tuners that can counterbalance actively transcribed genes to prevent the overwhelming activation of genes. To identify negative regulators that can calibrate the proper level of gene expression, we analyzed several data sets, including genome-wide RNAi screening using Oct4-GFP reporter, expression profiles of time-course differentiation of ES cells, and global protein-DNA interaction mapping of ES cell core TFs. Through integrative analysis with these data, we finalized the top 5 candidate factors (Gli1, Med26, Taf6, Etv4, and Rbpj). Most of these factors are associated with prenatal lethality in mice upon knockout, highlighting their biological significance. We confirmed that overexpression of the 5 factors in mouse ES cells decreased expression of ES cell core TFs, whereas the knockdown of the factors increased the levels of the core TFs, suggesting they can repress the activities of the core factors. Among the factors, Taf6, Etv4, Rbpj, and Med26 can directly bind the cis-regulatory element of core TFs. Gli1 and Rbpj physically interact with the ES cell core TFs and HDACs. These data collectively imply that the 5 factors bind ES cell core TFs and may recruit co-repressor such as HDACs to counterbalance the core TFs. In summary, we identified multiple transcriptional repressors that can fine-tune the expression levels of actively transcribed genes. This study provides a new insight into transcriptional regulation and potential therapeutic targets for diseases caused by the deregulation of gene expression programs.

P-22: Synthesis of Trifluoromethyl Substituted Isogemichalcone B and C Analogs

Andrew Yun, Graduate Student

Villanova University



Aromatase, a member of the cytochrome P450 family of enzymes, catalyzes the aromatization of androgen precursors, androstenedione and testosterone, to provide estrogen. Estrogen is responsible for the proper growth of tissues and bones. However, in post-menopausal women, production and storage of estrogen is downregulated, increasing the risk of breast cancer. The aromatization step is a key focal point that can be regulated to lower the risk of breast cancer in post-menopausal women. As part of a natural product screening effort, Kinghorn et al. discovered moderate aromatase inhibiting ability of Isogemichalcone B and C, metabolites isolated from the flowering weeds Hypercum geminiflorum and the mulberry tree Broussonetia papyrifera1. The completed total synthesis of Isogemichalcone B and C provided a variety of possible analogs with structure-activity relationships2. The focus of this work was to synthesize the trifluoromethyl substituted analogs of Isogemichalcone B and C. This involves use of key reactions explored in the synthesis of the original Isogemichalcone B and C, including the Stille cross-coupling, Claisen-Schmidt condensation, and Mitsunobu coupling. The trifluoromethyl substituted analog of Isogemichalcone B and C was synthesized in an overall 8.5% yield and 6.5% yield respectively.

P-23: Fusobacterium nucleatum promotes colorectal cancer by inducing Wnt/β-catenin modulator Annexin A1

Jung Eun Baik, Ph.D.

Memorial Sloan Kettering Cancer Center

Fusobacterium nucleatum, a Gram-negative oral anaerobe, is a significant contributor to colorectal cancer. Using an in vitro cancer progression model, we discover that F. nucleatum stimulates the growth of colorectal cancer cells without affecting the pre-cancerous adenoma cells. Annexin A1, a previously unrecognized modulator of Wnt/β-catenin signaling, is a key component through which F. nucleatum exerts its stimulatory effect. It is specifically expressed in proliferating colorectal cancer cells and involved in activation of cyclin D1. Annexin A1 expression level in colon cancer is a predictor of poor prognosis independent of cancer stage, grade, age and sex. The FadA adhesin from F. nucleatum up-regulates Annexin A1 expression through E-cadherin. A positive feedback loop between FadA and Annexin A1 is identified in the cancerous cells, absent in the non-cancerous cells. We therefore propose a “two-hit” model in colorectal carcinogenesis, with somatic mutation(s) as the first hit, and F. nucleatum as the second hit exacerbating cancer progression after benign cells become cancerous. This model extends the “adenoma-carcinoma” model and identifies microbes such as F. nucleatum as cancer “facilitators”.



KHIDI FORUM

“한국 바이오헬스산업 성장을 위한 미래 인재양성 방안” 프로그램

월일

(요일) 시간 주제 및 내용 발표자

11.1

(금)

5분

(13:00~13:05) ○ 개회사

홍승욱 팀장

(한국보건산업진흥원)

5분

(13:05~13:10) ○ 환영사

K. Stephen Suh 회장

(KASBP)

Session 1. 한국 바이오헬스분야의 인재양성 현황 – 특성화대학원 중심으로

10분

(13:10~13:20) Session 1-1. Pharmaceutical Industry in Korea

동영상

(한국보건산업진흥원)

15분

(13:20~13:35)

Session 1-2. 제약산업 특성화 대학원의 운영현황 및 성과, 향후

인재육성 방안

- 특성화 대학원 교육 체계 및 커리큘럼 소개

- 특성화 대학원 인재 양성방향 및 향후 과제 등

정진현 교수

(연세대학교)

15분

(13:35~13:50)

Session 1-3. 의료기기산업 특성화 대학원의 운영현황 및 성과,

향후 인재육성 방안

- 특성화 대학원 교육 체계 및 커리큘럼 소개

- 특성화 대학원 인재 양성방향 및 향후 과제 등

권지연 교수

(동국대학교)

10분

(13:50~14:00) Break Time

Session 2. 미국 바이오헬스분야의 주요 현황 및 글로벌 리더 양성

15분

(14:00~14:15)

Session 2-1. 미국 바이오헬스 신산업 현황 및 한국과 협력방안

- 미국 바이오헬스 트렌드분석을 통한 한미 협력방안 제언

우정훈 대표

(Mass. Biomed LAB)

15분

(14:15~14:30)

Session 2-2. 글로벌 기업에서 요구되는 인재상

- 글로벌 바이오 시장에서 원하는 인재상, 기업 요구수준 등

글로벌 제약사

(KASBP Leaders)

15분

(14:30~14:45)

Session 2-3. 차세대 리더로 성장하기 위한 노력방안

- 국내·외 교육 차이점, 한국 인재 양성 정책의 한계점 및 제언 등

유학생, PhD, YG leaders

and members 등

15분

(14:45~15:00) Break Time

Session 3. 바이오헬스분야의 글로벌 리더 양성을 위한 해외진출 방안

60분

(15:00~16:00)

Session 3-1. KASBP 전문가, 기업 및 대표단 토론회

- 글로벌 연수 프로그램 개발 및 협력방안 논의

- 국내 기업의 우수인재 유치 장 마련

- 실무중심 인재양성을 위한 프로그램 개발 및 지원 정책 아젠다

도출 등

특성화 대학원 교수진

KASBP

한국보건산업진흥원

KASBP Leaders providing presentations: K. Stephen Suh, Soo-Hee Park, Wooseok Han, Hyun-Hee Lee YG participants for the discussion: Sungki Kim, Hyelim Kim, Yoonji Baek, Jihyun Kim, Suhyun Lee, and Ji Eun Lee YG observer/input: Minsung Kang, Sangwoo Lee, Sehyun Kim



PAST FELLOWSHIP AWARDEES

KASBP-DAEWOONG ACHIEVEMENT

2009 Jong Eun KIM (Gilead Sciences, Inc.), (Kainos Medicine Inc, Korea, Current) 2010 David C. CHU, (University of Georgia) 2011 Sung Ho KIM (University of California, Berkeley) 2012 Dennis CHOI (Stony Brook Medicine and Stony Brook University) 2013 Joseph KIM (Inovio Pharmaceuticals) 2014 Kinam PARK (Purdue University) 2015 Jong Sung KOH (Genoscco) 2016 Jang-Ho CHA (Novartis) 2017 Peter PARK (Bicycle Therapeutics) 2018 Jong Wook LEE (Daewoong Pharmaceuticals)

KASBP RECOGNITION AWARD

2015 Jong Wook LEE (Daewoong) KASBP-DAEWOONG FELLOWSHIP

2006 JaeKi MIN (New York University), Hahn KIM (Princeton University), HyeJin PARK (Rutgers University) 2007 JiSook MOON (Harvard University), SungYeon PARK (Rutgers University), SeokGeun LEE (Columbia

University) 2008 HeungKyu LEE (Yale University), JungHwan KIM (Rutgers University), MinSik KANG (Columbia University) 2009 JinAh PARK (Harvard University), JaeMin CHOI (Yale University), DeokHo KIM (Johns Hopkins University) 2010 JungMin KEE (Rockefeller University), HyungWook KIM (NIH), SeJin AHN (Harvard University) 2011 MooRi HAN (University of California, LA), HwanJong JANG (Boston College) 2012 JeongHo JANG (Columbia University), JaeWoo CHOI (Oregon State University) 2013 JangEun LEE (University of Pennsylvania), Eun Chan PARK (Rutgers University) 2014 Kimberly H. KIM (Harvard University), Seung Koo LEE (Weill Cornell Medical College), Min-Sik KIM (Johns

Hopkins University) 2015 Jiyeon KIM (UT Southwestern), Sun Mi PARK (Memorial Sloan-Kettering Center); Byeong Seon KIM

(University of Pennsylvania) 2016 Sang Bae LEE (Columbia University), Junil KIM (University of Pennsylvania), Ho-Keun KWON (Harvard

Medical School) 2017 KyeongJin KIM (Columbia University Medical Center), Min-Ji BAK (Ernest Mario School of Pharmacy),

Heung Sik HAHM (Free University Berlin) 2018 Jung Ho HYUN (Max-Planck Florida Institute for Neuroscience), Seung Hoon LEE (Harvard Medical

School), Jang Hwan CHO (Boston University)

KASBP-GC Pharma (formerly GREEN CROSS) FELLOWSHIP

2011 HanSang CHO (Harvard Medical School), SungWoong KANG (Johns Hopkins University), MiYeon KIM (Columbia University), JaeYoung SOH (Rutgers University), SungYong HWANG (NIEHS/NIH)

2012 WonJin CHO (Drexel University), HyoJung KANG (Yale University), JungHyun LEE (Columbia University), YongJae LEE (Yale University), JaeHyun YOON (NIH)

2013 Yunjong LEE (Johns Hopkins University), Jun-Dae KIM (Yale University), Bae-Hoon KIM (Yale University), Ja Young KIM-MULLER (Columbia University)

2014 Catherine RHEE (University of Texas at Austin), Ji-Seon SEO (The Rockefeller University) Sehyun KIM (New York University)

2015 Young-Su YI (New York University), Hee-Woong LIM (University of Pennsylvania), Bloria Bora KIM (The Pennsylvania State University)

2016 Eui Tae KIM (University of Pennsylvania), Kihyun LEE (Weill Cornell Medical Science) 2017 Seung-Yeol PARK (Harvard medical school), Young Bok Abraham KANG (Harvard medical school)



2018 Jae Yeon HWANG (Yale University), Youngjin KIM (Rockefeller University) 2019 Hongsuk Park (Washington University School of Medicine in St. Louis), Byungyong Ahn (University of

Pennsylvania) KASBP-HANMI FELLOWSHIP

2011 HyungJin AHN (Rockefeller University), ChangHoon CHO (Abramson Research Center) 2012 YuNa KIM (University of North Carolina), HyunSeob TAE (Yale University), InHye LEE (NIH) 2013 JooHee LEE (Memorial Sloan-Kettering Cancer Center), KyungRyun LEE (Rutgers University), ManRyul LEE

(Indiana University) 2014 Young Chan CHA (Wistar Institute), Min-Kyu CHO (New York University), Lark Kyun KIM, (Yale University),

Yu Shin KIM (Johns Hopkins University) 2015 Seonil KIM (New York University), Peter B. KIM (Yale University) 2016 Sungwhan OH (Harvard Medical School), Won-Gil LEE (Yale University), Hee-Jin JEONG (Harvard Medical

School) 2017 Seungkyu LEE (Harvard Medical School), Soo Seok HWANG (Yale University), Heeoon HAN (University of

Pennsylvania) 2018 Jae Yeon HWANG (Yale University), Yeong Shin YIM (MIT), Dahea YU (Rutgers University) 2019 Seung Wook Kim (University of Texas at Austin), Kwang-Su Park (Ichan School of Medicines at Mt. Sinai),

Jooman Park (University of Massachusetts)

KASBP-LG CHEM FELLOWSHIP

2017 Kyoung-Dong KIM (Wistar Institute), Seok-Man HO (Icahn School of Medicine at Mount Sinai) 2018 Kisa SUNG (Icahn School of Medicine at Mount Sinai), Gihoon LEE (University of Chicago)

KASBP-QURIENT FELLOWSHIP

2018 Soeun KANG (University of Illinois at Chicago), Do Hyung KIM (Johns Hopkins University) KASBP-YUHAN FELLOWSHIP

2011 KiYoung KIM (Boston University), JoongSeop SHIM (Johns Hopkins University)

2012 YeMin HUH (University of Michigan), SookHee BANG (University of Pennsylvania), JungHo BAIK (Columbia University)

2013 Dong Jun LEE (University of Chicago), Ingyu KIM (Yale University), Ja Yil LEE (Columbia University)

2014 Seouk Joon KWON (Rensselaer Polytech Institute), Jeongmin SONG (Yale University), Jae-Hyun YANG (Harvard Medical School), Wan Seok YANG (Columbia University)

2015 Min-Joon HAN (Harvard Medical School), Minjung KANG (Cornell University)

2016 Ki Su KIM (Harvard Medical School), Hongjae SUNWOO (Harvard Medical School), Seo-Young PARK (University of Massachusetts)

2017 Hanseul YANG (Rockefeller University), Ji-Hoon PARK (NIH), Hong-Yeoul RYU (Yale University)

2018 Sangdoo KIM (Harvard Medical School), Baehyun SHIN (Harvard Medical School), Mikyung YU (Harvard Medical School)

2019 Hyunkyung Jung (University of Illinois at Urbana Chamgaign), Woosook Kim (Columbia University), Sungjoon Cho (University of Illinois at Chicago)

KASBP-ST PHARM FELLOWSHIP

2016 Jung-Eun JANG (New York University), Byungsu KWON (MIT) KASBP FELLOWSHIP

2009 SangHo CHOI (NIH) 2010 SangRyung KIM (Columbia University), TaeSook YOON (Rutgers University), EunMi HUH (Cal. Tech.)



2015 Mi Jung KIM (Duke University), Minyoung PARK (The Rockefeller University) 2018 Sinyoung JEONG (Harvard Medical School), Young Eun LEE (Monell Chemical Senses Center)

KASBP-KSEA FELLOWSHIP

2013 Sung In LIM (University of Virginia) 2014 Keun-woo JIN (Temple University)

KASBP-KUSCO FELLOWSHIP

2008 HyunHo KIM (National Institutes of Health), TaekBeom OHN (Harvard Medical School), WonAh JOO (Wistar Institute)

KASBP-KRICT FELLOWSHIP

2009 SeungSik SHIN (Rutgers University), EunJoo JEONG (Columbia University), KyuWon BAEK (University of Pennsylvania)

KASBP-KHIDI FELLOWSHIP

2010 JaeHyun BAE (Yale University), HeeYeon CHO (Boston College)

KASBP-DAEWOONG SCHOLARSHIP

2006 Jin K. PAI, Schering-Plough (Handok Pharmaceuticals, Korea, Current) 2007 YoungWhan PARK, Merck (National Cancer Center, Korea, Current) 2008 Young-Choon MOON (PTC Therapeutics) 2009 HongYong KIM (Novartis)

KASBP-SKBP FELLOWSHIP

2019 Jungeun Baik (Memorial Sloan Kettering Cancer Center), Jeongjoon Choi (Yale University)



2019 KASBP Fall Symposium Attendees

Last

name

First name 한글 이름 근무처 Affiliation Networking Group

Ahn Byungyong 안병용 University of Pennsylvania

Ahn Jae Eun 안재은 Pfizer, Inc. PK/PD/pre-clinical/Clinical Science:

AHN Yongho 안용호 Samsung Biologics

Aoyagi Kazuko Celerion BAE HYUN JIN

배현진 Harvard Medical School PK/PD/pre-clinical/Clinical Science:

Bae Jae Hyun 배재현 Voronoi Immuno-oncology/Autoimmune/Inflammatory

Bae Jin 배진형 Broad Institute Cell and Gene Therapy/Viral infection/Rare

disease Bae Jun-Seok

배준석 Massachusetts General Hospital Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Baek Jea Hyun 백재현 Biogen Inc. Immuno-oncology/Autoimmune/Inflammatory

Baek Yoonji 백윤지 MCPHS University Pharmacy

Baik Jungeun 백정은 Memorial Sloan Kettering

Cancer Center Immuno-oncology/Autoimmune/Inflammatory

Cha Young 차영 McLean Hospital/Harvard

Medical School Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Chang Hee chul 장희철 Daewoong America BD/Legal/VC:

Chang Kern 장건희 Janssen R&D Immuno-oncology/Autoimmune/Inflammatory

CHO Hangseo 조항서 MCPHS University Pharmacy

Cho Jaehoon 조재훈 Brown University PK/PD/pre-clinical/Clinical Science:

Cho Min-Kyu 조민규 Novartis Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative Cho Soonshin

조순신 LG Chem Immuno-oncology/Autoimmune/Inflammatory

CHO SUNG YUN 조성윤 Weill Cornell Medicine Pharmacy

Choe Yun H. 최윤 Lucas and Mercanti, LLP BD/Legal/VC:

Choi AHyun 최아현 Novartis Immuno-oncology/Autoimmune/Inflammatory

CHOI Angela Yeri 최예리 Samsung Biologics

Choi Barlgum 최밝음 Alexion Pharmaceuticals

Engineer PK/PD/pre-clinical/Clinical Science:

Choi ByungHeon 최병헌 MCPHS University Cell and Gene Therapy/Viral infection/Rare

disease Choi Daeun

최다은 MCPHS University (Massachusetts College of Pharmacy and Health Sciences)

Pharmacy

Choi Dayun 최다윤 MCPHS University Pharmacy

Choi Hwan Geun 최환근 B2SBio Chemistry

Choi Hyeong-wook 최형욱 Eisai Inc.

Choi Jeonghoon 최정훈 Yumanity Therapeutics

Choi Jun Young 최준영 Nitto Avecia Chemistry

Choi So Jung 최소정 Rutgers Pharmacy

Choi Sung Hugh 최성휴 Pinetree Therapeutics Immuno-oncology/Autoimmune/Inflammatory



Last

name


Choi Sungwook 최성욱 U mass medical school Cell and Gene Therapy/Viral infection/Rare

disease Choi Yewon

최예원 Genosco PK/PD/pre-clinical/Clinical Science:

Choi Younggi 최영기 Alkermes Immuno-oncology/Autoimmune/Inflammatory

Choi Yunggeun 최영근 Genosco Immuno-oncology/Autoimmune/Inflammatory

Choo Min-Kyung 추민경 Takeda Immuno-oncology/Autoimmune/Inflammatory

CHUN Sung Yong 전성용 Kyungdong University

Chung HaeWon 정해원 Asimov Cell and Gene Therapy/Viral infection/Rare

disease Chung Seung Wook

정승욱 Boehringer Ingelheim PK/PD/pre-clinical/Clinical Science:

Chung Seungwon 정승원 AbbVie Chemistry

Chung Yoomin BD Pharmacy Eom Taesun

엄태선 Skyhawk Therapeutics Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

HAHM HEUNG SIK 함흥식 U of virginia Chemistry

HAHM Sean 함성원 The Yakup Shinmoon

Han Dae Yale PK/PD/pre-clinical/Clinical Science: Han Jinah

한진아 Biodrone Therapeutics Inc. Cell and Gene Therapy/Viral infection/Rare disease

Han Muri GC Pharma Han Sangyeul

한상열 INGENIA THERAPEUTICS PK/PD/pre-clinical/Clinical Science:

Han Wooseok 한우석 Novartis Institutes for

BioMedical Research Chemistry

Han Yong-Hae 한용해 CJ Healthcare Immuno-oncology/Autoimmune/Inflammatory

Heo Keunjung Boston Children's Hospital/Harvard Medical School

Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

HONG Andy 홍승욱 KHIDI

Hong Jun Young 홍준영 Yale University Immuno-oncology/Autoimmune/Inflammatory

Hong Man Hyung 홍만형 KH Medical㈜

Hong Peter S. 홍성원 LG Chem Immuno-oncology/Autoimmune/Inflammatory

Huh Kevin Kyung Hwa 허경화 KPBMA BD/Legal/VC:

Huh Meena 허민아 UNITES inc. PK/PD/pre-clinical/Clinical Science:

Hur Jeong Hwan 허정환 Boston Children's Hospital Immuno-oncology/Autoimmune/Inflammatory

Hwang Ji Young 황지영 Torque Therapeutics Immuno-oncology/Autoimmune/Inflammatory

Hwang So-Young 황소영 Genosco Immuno-oncology/Autoimmune/Inflammatory

Im Eunju 임은주 Nathan S. Kline Institute/NYU

School of Medicine Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Jang Eun-Seok 장은석 KRIBB

Jang Hwanjong 장환종 Boehringer-Ingelheim Chemistry

Jang Hyeyeong 장혜영 MCPHS University Pharmacy

JEON Seng Ho 전승호 Daewoong Pharmaceutical Co.

Ltd. Cell and Gene Therapy/Viral infection/Rare disease

Jeong Jae Uk 정재욱 GSK Cell and Gene Therapy/Viral infection/Rare

disease



Last

name


Jeong Jin-Hyun 정진현 Yonsei University

Jeong Laina 정효연 MCPHS University Pharmacy

Jeong Seihwan 정세환 Icahn School of Medicine at

Mount Sinai Immuno-oncology/Autoimmune/Inflammatory

Jeong Sinyoung 정신영 Wellman Center for

Photomedicine, Massachusetts General Hospital, Harvard Medical School

Chemistry

JINN SARAH MERCK Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Jo Sunhwan SilcsBio Chemistry Jung Hee Kwon

정희권 위더스㈜

Jung Jennie 정찬양 Sanofi Genzyme

JUNG JENNIFER 정진숙 DAVINCITF Corp Immuno-oncology/Autoimmune/Inflammatory

Jung Jenny 정유경 Rutgers University Pharmacy

Kam Yoonseok Agilent Technologies Immuno-oncology/Autoimmune/Inflammatory Kang Hyunki

강현기 5047104593

Kang Jessica 강나은 CVS pharmacy Pharmacy

Kang Jongkyun 강종균 Harvard Medical School/BWH Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative Kang Minsung MCPHS University PK/PD/pre-clinical/Clinical Science: Kang Myeong Gyun

강명균 웰마커바이오㈜

Kang Pilsoo 강필수 Sanofi Cell and Gene Therapy/Viral infection/Rare

disease Kang seolhee

강설희 Weill cornell medicine Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

KEUM BO RAM 금보람 MCPHS university Pharmacy

Ki Dong Hyuk 기동혁 Dana-Farber Cancer Institute Cell and Gene Therapy/Viral infection/Rare

disease Kim Aina

김아인 MCPHS University Pharmacy

Kim Boyoung 김보영 Harvard Medical School Cell and Gene Therapy/Viral infection/Rare

disease Kim Dae-Shik

김대식 Eisai Chemistry

Kim Dongeun 김동은 MCPHS University Pharmacy

Kim Esther 김현지 UW Madison Immuno-oncology/Autoimmune/Inflammatory

Kim Eunha 김은하 NEBS

KIM EUNHEE CHUNG-NAM NATIONAL UNIVERSITY

Kim Gloria 김보라 University of Pennsylania Immuno-oncology/Autoimmune/Inflammatory

Kim GyuLee 김규리 Rutgers University

Kim Hakwon 김학원 경희대학교 국제캠퍼스 응

용화학과/글로벌의약품소재

개발연구센터

Immuno-oncology/Autoimmune/Inflammatory

Kim Hee Jung 김희정 MCPHS Pharmacy

Kim Hyelim MCPHS University PK/PD/pre-clinical/Clinical Science:



Last

name


Kim Hyung Cheol 김형철 Korea Research Institute of

Bioscience & Biotechnology

Kim Hyungchul 김형철 Novartis PK/PD/pre-clinical/Clinical Science:

Kim Hyunki Joslin Diabetes Center Kim Ilhoon

김일훈 GC녹십자 Cell and Gene Therapy/Viral infection/Rare disease

Kim Jaeah 김재아 Biogen PK/PD/pre-clinical/Clinical Science:

Kim Jae-Hun 김재훈 IFF Chemistry

Kim Jeong Yeon 김정연 KPBMA BD/Legal/VC:

Kim Jeong-Ki 김정기 Columbia University Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative Kim Ji-Hyun

김지현 MCPHS University Pharmacy

Kim Jisun 김지선 Mclean Hospital Cell and Gene Therapy/Viral infection/Rare

disease Kim Joonyul

김준열 Ciscovery Bio PK/PD/pre-clinical/Clinical Science:

Kim Juhee 김주희 Northeastern University Pharmacy

Kim Juhyun UCLA Cell and Gene Therapy/Viral infection/Rare disease

Kim Juny 김주은 CRScube America BD/Legal/VC:

Kim Kevin 김재훈 Sarepta Therapeutics Cell and Gene Therapy/Viral infection/Rare

disease Kim Kwang Soo

김광수 McLean Hospital/Harvard Medical School

Cell and Gene Therapy/Viral infection/Rare disease

Kim Kyung 김경효 AbbVie

KIM Kyungae 김경애 Kyungdong University

Kim Kyusik 김규식 University of Massachusetts

Medical School Cell and Gene Therapy/Viral infection/Rare disease

Kim Lily Spaulding Hospital Pharmacy Kim Meehyein

김미현 Korea Research Institute of Chemical Technology

Cell and Gene Therapy/Viral infection/Rare disease

Kim Mijeong 김미정 The University of Texas at Austin Cell and Gene Therapy/Viral infection/Rare

disease Kim Mi-Sook Takeda PK/PD/pre-clinical/Clinical Science: Kim Nam-Cheol

김남철 United States Pharmacopeia Pharmacy

Kim Nami 김남이 BIDMC (Harvard medical

school) Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Kim Sang-Hun 김상헌 Yale school of medicine Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative Kim Sarah

김사라 Law Offices of Sarah Kim, LLC PK/PD/pre-clinical/Clinical Science:

Kim Seyoon 김세윤 Samyang Biopharm USA BD/Legal/VC:

Kim Soyun 김소연 Walgreens Pharmacy

Kim Su Kim Sun Wook

김선욱 Brigham and Women's Hospital/Harvard Medical School

Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Kim Sun Young 김선영 Wellmarkerbio

Kim Sung ki 김성기 MCPHS university BD/Legal/VC:

Kim Sung-Kwon Alexion Pharmaceuticals Immuno-oncology/Autoimmune/Inflammatory



Last

name


Kim Sunhwa Merck Research Laboratory (Merck & Co, Inc)


Kim Taeg 김 택수 Jnana Therapeutics Immuno-oncology/Autoimmune/Inflammatory

Kim Taewoo 김태우 Mclean hospital

Kim Woori 김우리 McLean Hospital/Harvard

Medical School

Kim Woosook 김우숙 Columbia University Medical

Center Immuno-oncology/Autoimmune/Inflammatory

Kim Yoon Gi 김윤기 Widenpartners BD/Legal/VC:

Kim Young Ju 김영주 Northeastern University Pharmacy

Ko KyuJung(Henry) 고규정 피플앤박컨설팅/KJ컨설팅

Koh Eun-Ik 고은익 University of Massachusetts


Koh Hyunyong 고현용 Boston Children's Hospital PK/PD/pre-clinical/Clinical Science:

Koo Ja Rok 구자록 University of Ulsan

Kwon Byungsu 권병수 MIT chemistry Chemistry

Kwon Hyunah 권현아 MCPHS

Kwon Ji yean 권지연 Dongguk University

Leblanc Pierre McLean Hospital Cell and Gene Therapy/Viral infection/Rare disease

Lee Chang-Sun (Sam) 이창선 Legochem Bio Immuno-oncology/Autoimmune/Inflammatory

LEE DAE-HEE 이대희 강릉원주대 생명과학대 Immuno-oncology/Autoimmune/Inflammatory

Lee Hak-Myung Shire Cell and Gene Therapy/Viral infection/Rare disease

Lee Hongwon 이홍원 KRIBB

Lee Hyun-Hee Merck Immuno-oncology/Autoimmune/Inflammatory Lee Hyunkyung

이현경 MCPHS University Pharmacy

Lee Jae Won 이재원 ㈜티카로스

LEE JAEKYOO 이재규 GENOSCO Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative Lee Jaemoon Agios Pharma Inc. Lee Jane

이지윤 Northeastern University Pharmacy

Lee JangEun 이장은 Boehringer Ingelheim Immuno-oncology/Autoimmune/Inflammatory

Lee Ji Eun 이지은 MCPHS University BD/Legal/VC:

Lee Jong Wook 이종욱 Daewoong Pharmaceutical Co.

Ltd. Immuno-oncology/Autoimmune/Inflammatory

Lee Jooyoung 이주영 University of Massachusetts


LEE JU-HYUN 이주현 Nathan Kline Institute/NYU

Langone Medical Center Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Lee Jung Hwa 이정화 Cambridge MA Chemistry

Lee Jungeun "Cindy" 이정은 Northeastern University Pharmacy

LEE Kang-Won Wayne 이강원 The University of Rhode Island

Fascitelli Center for Advanced Engineering

LEE Kyuhwan 이규환 KHIDI



Last

name


Lee Namgyu 이남규 Univeristy of Massachusetts


Lee Sangwoo 이상우 MCPHS University Pharmacy

Lee Suhyun MCPHS University Pharmacy Lee Sung joo Orum Therapeutics Immuno-oncology/Autoimmune/Inflammatory Lee Tae Hoon

이태훈 Kyung Hee University

Lee WonGil 이원길 Genosco Chemistry

Lee WonGil 이원길 Genosco Chemistry

LEE Young-suk 이영석 Kyungdong University

Lim Hanjo 임한조 Genentech PK/PD/pre-clinical/Clinical Science:

Min Jiyoung 민지영 GSK

Min Soohong 민수홍 Harvard Medical School

Moon Dawn 문다은 Northeastern University

Na Ha Eun 나하은 MCPHS Pharmacy

Na Insung 나인성 LORENZERIK, Inc.

Nam Suah 남수아 MCPHS University Worcester

Campus Pharmacy

Nam Younjong 남연종 MCPHS University Pharmacy

Nayeon Lee 이나연 Mclean hospital

Oh Jaetaek 오재택 GC pharma Cell and Gene Therapy/Viral infection/Rare

disease Oh Richard Novo Nordisk Pharmacy Oh Sang Cheul

오상철 Korea University Guro Hospital BD/Legal/VC:

Oh Seung Wook 오승욱 Biodrone Therapeutics Inc. Cell and Gene Therapy/Viral infection/Rare

disease Oh Sungwhan

오성환 Brigham and Women's Hospital / Harvard medical school


Oh Younghoon 오영훈 Spark Therapeutics Cell and Gene Therapy/Viral infection/Rare

disease Pai Sanghoon

배상훈 kyunghee univ.

Paik Donggi 백동기 Harvard Medical School

Paik Ik-Hyeon 백익현 WAVE Life Sciences, Inc. Chemistry

Park Goonho Goonho Park

UCSD Respiratory/metabolic/cardiovascular/Aging/mental/Neurogenerative

Park Hannah 박한나 MCPHS Pharmacy

Park Hye-jin 박혜진 CUNY-ASRC

Park Jeehae 박지혜 Sanofi Cell and Gene Therapy/Viral infection/Rare

disease Park Jin Seon Charles River Laboratories Cell and Gene Therapy/Viral infection/Rare

disease Park Jo Eun

박조은 MCPHS University Pharmacy

PARK JONG KUK 박종국 KIRAMS Immuno-oncology/Autoimmune/Inflammatory

Park Jongho 박종호 HMS/MGH

Park Jonghoon 박종훈 LG Chem Life Sciences

Innovation Center, Inc. Immuno-oncology/Autoimmune/Inflammatory



Last

name


Park Joon Seok 박준석 대웅제약 Immuno-oncology/Autoimmune/Inflammatory

Park Julius 박태헌 None Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative Park Jungmin

박정민 MCPHS University Pharmacy

Park Kihyo 박기효 GC Pharma (녹십자)

Park Kwang-Su 박광수 Icahn school of medicine at

Mount Sinai

Park Minyoung 박민영 Daewoong Pharmaceutical Immuno-oncology/Autoimmune/Inflammatory

Park no-suk 박노석 People&Park Consulting BD/Legal/VC:

Park Sangho 박상호 University of Michigan Medical

School Immuno-oncology/Autoimmune/Inflammatory

Park Sehyun 박세현 MCPHS University Pharmacy

Park Seoin 박서인 MCPHS Pharmacy

Park Seong Ju 박성주 Cape Cod Hospital Pharmacy

Park Soo-Hee Novartis Cell and Gene Therapy/Viral infection/Rare disease

Park Sung Jin 박성진 Univeristy of Massachusetts


Park Sungyong 박성용 IPON Boston, Inc. BD/Legal/VC:

Park Tae-Yoon 박태윤 McLean Hospital Immuno-oncology/Autoimmune/Inflammatory

Rhee So Hyun 이소현 Rutgers University MBA Cell and Gene Therapy/Viral infection/Rare

disease Rim Nicholas

임내균 Novartis PK/PD/pre-clinical/Clinical Science:

RYU Jong Sang 유종상 Daewoong Pharmaceutical Co.

Ltd. Cell and Gene Therapy/Viral infection/Rare disease

Seo Joon 서준호 Rutgers University PK/PD/pre-clinical/Clinical Science:

Seo Kab 서갑식 Bushitol Corporation

Shin Hyunjin (Gene) 신현진 Takeda Pharmaceuticals

Shin Kkot-shi-gye 신꽃시계 Ministry of Health and Welfare

Shin Yong Hwan 신용환 KRIBB

Sohn Jihee Biogen PK/PD/pre-clinical/Clinical Science: Son Woo Jae

손우재 위더스㈜

Song Hojuhn 송호준 Pinetree Therapeutics, Inc BD/Legal/VC:

SONG JI YUN 송지윤 PH-PHARMA Cell and Gene Therapy/Viral infection/Rare

disease SUH BYUNG-CHUL

(Ben) 서병철 Enanta Pharmaceuticals, Inc Chemistry

Suh K. Stephen Kwangsun Suh

DiagnoCine Immuno-oncology/Autoimmune/Inflammatory

Suh Sandy Exeltis PK/PD/pre-clinical/Clinical Science: Sung Kisa

성기사 Icahn School of Medicine at Mount Sinai

Pharmacy

Sung Moo Je 성무제 Novartis Immuno-oncology/Autoimmune/Inflammatory

Sunwoo Hongjae 선우홍재 Intellia Therapeutics Cell and Gene Therapy/Viral infection/Rare

disease Won Doyon

원도연 Fish & Richardson PC BD/Legal/VC:



Last

name


Won Hee Mok 원희목 한국제약바이오협회

(KPBMA)

BD/Legal/VC:

Woo Janghee Novartis Immuno-oncology/Autoimmune/Inflammatory Woo Jung-hoon

우정훈 Mass Biomed Lab

Woo Jung-hoon 우정훈 Mass Biomed Lab

Woo Sangsoon 우상순 Cytel PK/PD/pre-clinical/Clinical Science:

YANG Eun Young 양은영 Samsung Biologics

Yang Heeyoon 양희윤 UW-Madison Immuno-oncology/Autoimmune/Inflammatory

Yang Jae-Hyun 양재현 Harvard Medical School Respiratory/metabolic/cardiovascular/Aging/me

ntal/Neurogenerative YANG JINYOUNG

양진영 LG Chem Immuno-oncology/Autoimmune/Inflammatory

Yang SEUNGCHAN 양승찬 RES Group PK/PD/pre-clinical/Clinical Science:

Yi Jae Kyo 이재교 Harvard Medical School/Dana-

Farber Cancer Institute Immuno-oncology/Autoimmune/Inflammatory

Yim HyeRin 임혜린 Icahn school of medicine at

Mount Sinai Pharmacy

Yim Sang Hyuk 임상혁 MCPHS-Worcester Pharmacy

Yoon Donghoon 윤동훈 UAMS Immuno-oncology/Autoimmune/Inflammatory

Yoon Hojong 윤호종 Harvard Medical School/ Dana-

Farber Cancer Institute Chemistry

Yoon Hyokyung 윤효경 MCPHS University Pharmacy

Yoon Seung Won 윤승원 Rutgers Pharmacy

Yoon Sunggeun 윤성근 KHIDI

Yoon Taewon 윤태원 유한 USA (Boston office) Immuno-oncology/Autoimmune/Inflammatory

Yu Mikyung 유미경 Alnylam Pharmaceuticals Cell and Gene Therapy/Viral infection/Rare

disease Yun Andrew

윤석재 Chemistry

2019 KASBP Fall Symposium Sponsors

rev 2019 kasbp fall symposium program final

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