Reaching new heights in cancer treatmentsInnovative approaches for a wide range of cancers

MARCH 2018

Advancing the Treatment of Cancer Through Targeted Therapeutics

▪ When used anywhere in this presentation, whether oral or written, the words expects, believes, anticipates, estimates and similar expressions are intended to identify forward-looking statements. Forward-looking statements may include statements addressing future financial and operating results of Cotinga Pharmaceuticals (Cotinga).

▪ Cotinga bases these forward-looking statements on its current expectations about future events. Such statements are subject to risks and uncertainties including, but not limited to, the successful implementation of Cotinga’s strategic plans, the acceptance of new products, the obsolescence of existing products, the resolution of potential patent issues, competition, changes in economic conditions, and other risks described in Cotinga’spublic documents such as press releases and filings with the Toronto Stock Exchange and the Ontario Securities Commission.

▪ All forward-looking statements are qualified in their entirety by the cautionary statements included in this document and such filings. These risks and uncertainties could cause actual results to differ materially from results expressed or implied by forward-looking statements contained in this presentation. These forward-looking statements speak only as of the date of this presentation.

Disclaimer2

Clinical stage biotech company focused on the development of novel therapeutics for the treatment of cancers and other unmet medical needs

▪ Lead drug candidate is COTI-2, targeting p53− Completed dose escalation portion of Phase 1 trial for the treatment of

gynecological malignancies

• Promising safety, tolerability, PK, and PD readouts

− Initiated expansion arm of Phase 1 trial for the treatment of head and neck squamous cell carcinoma (HNSCC)

▪ Second drug candidate is COTI-219, targeting KRAS− Currently in IND-enabling studies− IND filing expected in 2018

▪ Pipeline-generating CHEMSAS® platform – in silico high throughput screening for molecule assessment

Publicly traded company TSX-V: COT

OTCQB: COTQF

Company and Pipeline Synopsis3

Cotinga Pipeline: Internally Discovered & Owned4

COTI-2: Potential Best-In-Class Therapy Targeting p53 in Multiple Oncology Indications

▪ In response to cellular stress, wildtype p53 induces cell cycle arrest and/or apoptotic cell death

▪ Mutant p53 promotes tumor formation (loss of tumor suppressor function)

– Mutant p53: single most important cancer-causing gene mutation known

– Most frequently mutated gene in human cancer implicated in >50% of all human cancers

▪ COTI-2 induces a wildtype-like conformational change in the p53 mutant protein thus restoring wildtype functional activity

– Oral small molecule

– Low preclinical toxicity

– Active as a mono or combination therapy

– Phase I in gynecological malignancies complete, initiated in head and neck cancer

mutp53mutp53

Sequence-specific transactivation defective

Conformational change to a wild-type configuration

Restoration of sequence-specific transcriptional activity

Apoptosis, growth arrest, senescence

mutp53

Drug Drug

COTI-2: Halting Mutant p53 Carcinogenesis 6

▪ COTI-2 induces a ‘wildtype-like’ conformational change in mutant p53R175H in TOV-112D ovarian cancer cell line but has no effect on p53WT conformation in H460 NSCLC cell line

▪ Similar results with multiple p53 mutant proteins in other constructs from HCT-116 colorectal cancer cell line

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Mutant p53 Levels in the Presence/Absence of COTI-2Wildtype p53 Levels in the Presence/Absence of COTI-2

Conformational change of mutant p53 to wildtype-like No effect on wildtype p53 protein levels

COTI-2 Specifically Targets Mutated p53 Mechanism7

▪ COTI-2, administered IV and PO, produced a significant tumor growth inhibition as a single agent in an OVCAR-3 ovarian cancer xenograft model

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Group 1 = Vehicle IV

Group 2 = COTI-2 20mg/kg IV

Group 3 = COTI-2 40mg/kg IV

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Group 4 = Vehicle PO

Group 5 = COTI-2 75mg/kg PO

Group 6 = COTI-2 100mg/kg PO

Significant Tumor Growth Inhibition as a Single Agent8

▪ Oral COTI-2 administration produced significant tumor growth inhibition in the HCT-116 p53G245C colorectal cancer cell line construct

▪ No effect in a HCT-116 (GFP) construct without p53 mutation

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COTI-2 (75 mg/kg)

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Target Specific Tumor Growth Inhibition as a Single Agent9

Gynecological malignancies:– ~100,000 patients are diagnosed with gynecological cancer per year; disease affects

~1.2M women in total (US)– Mutant p53 occurs in ~50% of recurrent disease (~15-20,000 patients per year) and in

~96% of high-grade serous ovarian cancer– Current standards of care (surgery, radiation, chemotherapy) associated with

increased morbidity and high toxicity

COTI-2 Gynecological Malignancies Clinical Trial Design:– Primary objectives:

▪ Evaluate the safety and tolerability of COTI-2▪ Determine Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose

(RP2D) of COTI-2

– Secondary objective: Evaluate pharmacokinetics, clinical activity, and responseduration of COTI-2

– Exploratory objectives:▪ Determine if baseline molecular aberrations correlate with activity of COTI-2▪ Evaluate pharmacodynamic markers of COTI-2 activity

COTI-2 Phase 1 in Gynecological Malignancies10

COTI-2 Phase 1 Primary Objective: Safety & Tolerability

Evaluate the safety and tolerability of COTI-2

– 24 patients were enrolled with ovarian, fallopian tube, endometrial or cervical cancers for which no effective or curative measures existed, with a median age of 60 and a median of 5 previous courses of chemotherapy

– COTI-2 was safe and well tolerated at increasing dose levels between 0.25 - 1.7 mg/kg

▪ Most common drug-related Adverse Events (AEs) were nausea and vomiting, fatigue and abdominal pain

Determine Maximum Tolerated Dose (MTD) and Recommended Phase 2 Dose(RP2D) of COTI-2

– MAD of 1.7 mg/kg and MTD/RP2D of 1.0 mg/kg established (based on 5 days/week, oral dosing)

11

Cohort t1/2 (hr) Tmax (hr)Cmax

(ng/mL)

AUC0-t

(ng∙hr/mL)

AUC0-∞

(ng∙hr/mL)

1 6.5 1.18 69 396 435

2 9.0 1.16 122 651 767

3 9.1 0.83 337 1489 1765

4 8.6 1.31 245 1331 1534

COTI-2 PK parameters by cohort

• Highest concentrations of COTI-2 approximately 1 hour after dosing

• T1/2 8-10 hours; substantially longer than other treatments targeting mutant p53

• No evidence of long-term drug accumulation

• Washout in approximately one week after last dose

Secondary Objective: Pharmacokinetics 12

Exploratory Objective: Pharmacodynamics

▪ 24 patients were enrolled with ovarian, fallopian tube, endometrial or cervical cancers for which no effective or curative measures existed, with a median age of 60 and a median of 5 previous courses of chemotherapy

▪ 15 patients were evaluated for Secondary and Exploratory outcome measures, including signals of efficacy using RECIST1 criteria.

– 11 of the 15 patients had ovarian cancer

– 12 of the 15 patients were genetically-profiled, and 9 of the 12 exhibited p53 mutations

– 1 of the 15 patients was determined to have overall stable disease

– 4 of the 15 patients were determined to have progressing disease but stable target lesions

– 5 of the 15 patients were determined to have progressing disease but stable non-target lesions

– 1 patient was observed to have a decrease in Cancer Antigen-125 (CA-125) levels in her blood

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COTI-2 Phase 1 HNSCC trial:

▪ Clinical trial site – MD Anderson Cancer Center

▪ Initial safety and tolerability trial initiated: first cohort started at 1.0 mg/kg

▪ Primary (cohort 1-3) readout expected in Q2 2018

Head and Neck Small Cell Carcinoma (HNSCC):

▪ ~65,000 patients are diagnosed with head and neck squamous cell carcinoma(HNSCC) per year; disease predominantly affects men, with approximately447,000 patients identified (US)

▪ ~40-50% HNSCC associated with mutant p53

▪ Current treatments include surgery, radiotherapy and chemotherapy

▪ Approximately 13,000 deaths from HNSCC in the US per year, representing aclear unmet need for additional treatment options

COTI-2 Phase 1 Trial in Head and Neck Cancers Initiated 14

Robust in vitro Data for COTI-2 Combination in HNSCC

▪ Isobolograms for two PCI13 cell lines show strong synergy for COTI-2 + cisplatin

– combination data points all below additive curve lines

15

Significant Tumor Growth Inhibition in Combination Chemotherapy

▪ COTI-2, as a single agent and in combination with cisplatin, produced significant tumor growth inhibition relative to untreated controls in the PCI13 pG245D head and neck cancer xenograft models

▪ Cisplatin treatment alone did not yield significant tumor growth inhibition

(p53 G245D)

16

▪ COTI-2, whether as a single agent (75 mg/kg PO) or in combination with radiation, produced tumor growth inhibition relative to untreated controls in PCI13 pG245D, the p53-mutated head and neck cancer cell line

– COTI-2 + radiation (2 Gy) has better tumor suppression and tumor cure effect compared with COTI-2 or radiation alone

– Tumor growth regression was as follows: COTI-2 alone (1/6), radiation alone (1/6), COTI-2 + radiation (4/7)

Synergistic Tumor Growth Inhibition in Combination with Radiotherapy

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COTI-2 Combinations in Multiple Indications18

▪ + platins vs. SCLC

▪ + taxanes vs. SCLC, endometrial, pancreatic

▪ + nucleoside analog (gemcitabine) vs. pancreatic

▪ + mTOR inhibitor vs. glioblastoma

▪ + EGFR inhibitors (erlotinib, cetuximab) vs. colorectal

normalizing p53 function is expected to synergize with chemotherapy

PLoS One. 2018 Jan 24;13(1). PMID: 29364966. Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines.

COTI-2 Effective in Resistant Cancer Cells19

▪ with repeated exposure, SCLC and NSCLC cells acquired resistance to platins and taxanes but not to COTI-2

▪ SCLC and NSCLC cell lines with resistance to taxanes or platins were still sensitive to COTI-2

multiple chemo-resistant cell lines are sensitive to COTI-2

PLoS One. 2018 Jan 24;13(1). PMID: 29364966. Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines.

• Novel p53-dependent mechanism of action

• High oral bioavailability demonstrated in the patient population

• Low toxicity in preclinical and early clinical development

• High preclinical efficacy demonstrated

• Opportunity for single agent and combination therapy

• No drug resistance observed

• Sensitization to radiation therapy

• Granted FDA orphan drug status for ovarian cancer

• Strong IP protection in place - 8 U.S. patents issued

- 1 Japanese, 1 Canadian and 1 EU patent issued

- Additional patents pending

COTI-2 Best-in-Class Potential 20

COTI-219:Therapy Targeting KRAS in Multiple Oncology Indications

▪ KRAS proteins are signal switch molecules that regulate cell fates by coupling

receptor activation to downstream effector pathways

– Over-activation of RAS occurs in ~30% of human cancers

– KRAS mutations are prevalent in pancreatic, colorectal, endometrial,

biliary tract, lung and cervical cancers

▪ Malignant activation of KRAS promotes carcinogenesis

▪ COTI-219 prevents the activation of KRAS

– Oral small molecule

– Low preclinical toxicity

– Currently in preclinical development

KRAS-GTPON

KRAS-GDPOFF

GEF

GAP

Quiescence Cell Death

Proliferation SurvivalAngiogenesis

COTI-219 Prevents Activation of KRAS

COTI-219: Inhibits Oncogenic KRAS Over-Activation22

▪ COTI-219 inhibits KRAS activation

– Inhibition is time- and concentration-dependent

– This inhibitory effect is also evident in downstream targets

CELL LINEDURATION OF COTI-219

EXPOSURE (days)IC50 (nM)

HeyA8

1 10,000

3 72

5 50

7 55

CELL LINEDURATION OF COTI-219

EXPOSURE (days)IC50 (nM)

OVCAR8

1 10,000

3 N/A

5 79

7 47

HeyA8 Cell Line OVCAR8 Cell Line

COTI-219 Inhibits KRAS Activation23

▪ COTI-219 demonstrates single agent efficacy greater than standard chemotherapeutics in SHP-77 (KRASG12V) mouse xenograft model

▪ COTI-219 significantly inhibits tumor growth in the SHP-77 cells relative to vehicle control

Effect of Treatment on Tumor Volume

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TGI~80%

* All animals died

COTI-219 Significantly Inhibits Mutant KRAS Tumor Growth24

▪ KRAS-dependent mechanism of action (effective against mutant KRAS)

▪ Orally bioavailable and effective at low dose

▪ Low toxicity in preclinical development

▪ Opportunity for single agent and combination therapy

▪ No drug resistance observed

▪ Strong IP protection in place

– 5 patents in the U.S., Canada, Japan and select EU countries

COTI-219 Best-in-Class Potential 25

Corporate Update

COMPLETED

CORPORATE✓ Opened US office✓ Raised ~$4M CDN✓ Recapitalized equity structure✓ Rebranded from Critical Outcome Technologies to

Cotinga Pharma

COTI-2✓ Entered into first-in-human clinical trial✓ Completed dose escalation portion of Phase 1 trial

in gynecological malignancies at MDACC and NWU✓ Published two scientific articles on COTI-2✓ Launched HNSCC expansion arm in Phase 1 dose

escalation trial✓ Announced promising safety, tolerability, PK and PD

data from Phase 1 trial in gynecologicalmalignancies, including MTD and R2PD

COTI-219✓ Designated COTI-219 as next clinical candidate for

development✓ Initiated GMP manufacturing and IND-enabling

studies

UPCOMING

CORPORATE▪ Strengthen the balance sheet to execute on

corporate strategies▪ Opportunistically pursue regional or co-

development partnerships for COTI-2,pipeline programs and other technologies

COTI-2▪ Complete additional exploratory endpoint

data analysis for dose escalation portion ofPhase 1 trial in gynecological malignancies

▪ Complete Phase 1 dose escalation trial inHNSCC

▪ Initiate combination trials with COTI-2▪ Initiate p53 basket trial with COTI-2▪ Initiate breast cancer trial with COTI-2

COTI-219▪ File IND in 2018▪ Launch first-in-human trial in 2018

Corporate Objectives 2017-201827

Dr. Gordon Mills from the University of Texas MD Anderson Cancer Center, Houston, TX, Chairman

Dr. Douglas Levine from the Memorial Sloan-Kettering Cancer Center, New York City, NY

Dr. David Parkinson from New Enterprise Associates, Menlo Park, CA

Dr. Marshall Strome from the Center for Head and Neck Oncology at Roosevelt St. Luke's Hospital, New York City, NY

Dr. Nancy Chang, President, Apex Enterprises, Inc, and adjunct professor at the Departments of Medicine and Genetics at Baylor College of Medicine, Houston, TX

Robust Scientific Advisory Board28

MANAGEMENT TEAM

Alison Silva, MSc

▪ President & CEO

▪ Co-founder, former EVP & COO, Synlogic▪ Co-founder & Principal, The Orphan Group

Richard Ho, MD, PhD

▪ Chief Scientific Officer

▪ EVP R&D, Marina Biotech▪ Director, Disease Simulation, J&J PRD

Gene Kelly

▪ Chief Financial Officer

Kowthar Salim, PhD, MBA

▪ Vice President, Development

Debi Sanderson, MBA

▪ Director, Resourcing and Operations

DIRECTORS

John Drake, LLB, Chairman

▪ Chairman, Whippoorwill Holdings Limited

Alison Silva, MSc, President & CEO

Douglas Alexander, CPA, CA

▪ Chairman, Hydrogenics Corporation

Dave Sanderson, LLB

▪ Co-founder and President, Red Jacket Capital Inc.

John Yoo, MD FRCPC

▪ Professor of Oncology and Professor of Otolaryngology – Head and Neck Surgery at Western University; Co-chair of Cancer Care Ontario Head and Neck Disease Site

Experienced Leadership29

Trading

TSX Venture (2) COT

Recent closing price (3) $0.96

52 week range (3) $0.90 - 6.40

Market capitalization (3) $16,019,489

Capital

Cash (4) $1.25 M

Basic shares outstanding (3) 16,686,968

Options outstanding (3) 1,433,368

Warrants outstanding (3) (5) 3,824,242

Fully diluted shares outstanding (3) 21,944,578

Board & management control (3) (6) 12.3%

(1) All $ amounts in CAD(2) COTI also trades on the OTCQB as COTQF but amounts are for the TSXV only(3) As of the close of business Jan 17, 2018(4) As at Oct 31, 2017 consisting of cash, cash equivalents and investments(5) Includes warrants accounted for as warrant liabilities under IFRS(6) On a fully diluted basis

Key Company Facts

Contact:

Alison SilvaPresident & CEOOffice: (519) 858-5157Mobile: (860) 798-0816asilva@cotingapharma.com

Richard HoChief Scientific OfficerOffice: (858) 465-6139Mobile: (619) 884-8910rho@cotingapharma.com