neuroscience research peptides · neuroscience research peptides alzheimer’s disease quick...

1-800-777-4779 E-mail: [email protected]

Phone: 502-266-8787 Fax: 502-267-1329

P.O. Box 99703Louisville, KY 40269-0703 USA

Peptides International, Inc.

Neuroscience Research PeptidesAlzheimer’s Disease Quick Reference

Peptides International has a wide range of products of interst to the neuroscience researcher. These in-clude everything from peptide toxins such as Guangxitoxin-1E, Dendrotoxin, Conotoxin to the focus of this quick reference, Amyloid-Beta protein related peptides for Alzheimer’s research. Along with broad as-sortment of peptides and peptide-related offering, Peptides International also provides its custom peptide

synthesis services.

Normal Condition

γ- Secretaseα- SecretasePEN-2

AphNicastrin

Presenilin}

APP Intracellular

DomainAICD

Nuclear Translocation Transcriptional Regulation

Increased Neuronal Survival,

Neutrite Outgrowth, Synaptic sAPPα Plasticity,

Cell Adhesion

Glucose Transporters

NMDAR AMPAR

Acetylcholine Receptors:

nAChR mAChR

Ca2+Na+

Glc

•••

••

Normal Axon Pruning

Casp-6

Apoptosis

APPDR6

sAPPa

β- Secretase

Destabilized Microtubules

Aberrant Neuronal Death

Casp-6

Apoptosis

sAPPβ

Glucose Transporters

NMDARAMPAR

nAChR mAChR

Disease State

APPAPP

Amyloid Plaques Aβ Misfolding, Aggregation

ROS Formation

Casp-3,-9

Apoptosis

p53, Bad, Bax Production

& Activation

CytokinesRelease

Ac

MeP

Oxidative Stress

Activation of PKC, PKA, Erk2

Aβ40/42

Hyperphosphorylation of Tau

Lipid Peroxidation

Membrane Damage

N-APP

Neurofibrillary Tangles

Apoptosis

CDK5

p35

Akt

GSK-3α/β

Calpain

N-APP

p25

PPTau

γ- Secretase

AICD

γ- Secretaseβ- Secretase

DR6

Microglia Activation

Normal State of NeuronsAlzheimer’s Disease

ROS Formation

Alzheimer’s disease, a chronic neurodegenerative disease, affects more than 5 million people in the United States. It accounts for over $236 billion in medical care and is expected to rise to $1.2 trillion in 2050. It is the sixth leading cause of death in the US.

Alzheimer’s disease is a progressive brain disorder that causes problems with memory, thinking and behavior. Extracellular amyloid plaques and intracellular neurofibrillary tangles are hallmark features of Alzheimers disease.

Bulk material of our “Amyloid β-Protein (Human, 1-40)” is synthesized in trifluoroacetate form. Vials of this peptide (PAB-4307-v and PAB-4379-v), described as “Trifluoroacetate Form” and “HCl Form” are then prepared by lyophilization from DMSO and dilute HCl solution, respectively. Characteristic features of these vials, which are analyzed by CD in aqueous buffer at pH 7.4 and 37 °C (peptide concentration = 10 µM), are shown at right.

Lyophilized from DMSO Dilute HCl

Amyloid β-Protein (Human, 1-40)(Bulk, Trifluoroacetate Form)

PAB-4307-vAmyloid -Protein (Human, 1-40)

(Trifluoroacetate Form)

PAB-4379-vAmyloid -Protein (Human, 1-40)

[HCl Form]

Structure: Random Coil(for up to 24 h)

Structure Change: Random Coil(within 24 h)

β-Structure


Phone: 502-266-8787 Fax: 502-267-1329



CODE PRODUCT QTY

AMYLOID β PEPTIDES

PAB-4370-v Amyloid β-Protein (Human, 1-43) [TFA Form](Trifluoroacetate Form) Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala- Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala-Thr(M.W. 4615.1) C207H318N56O62SMajor Plaque Component in Alzheimer’s DiseasePurity: higher than 95% by HPLC

0.5 mg vial

PAM-4349-v Amyloid β-Protein (Human, 1-42) [TFA Form](Trifluoroacetate Form) Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val- Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala(M.W. 4514.0) C203H311N55O60SMajor Plaque Component in Alzheimer’s DiseasePurity: higher than 95% by HPLC

0.5 mg vial

PAB-4367-v [Pyr3]-Amyloid β-Protein (Human, 3-42) [TFA Form](Trifluoroacetate Form) Pyr-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser- Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala(M.W. 4309.9) C196H299N53O55SMajor Plaque Component in Alzheimer’s Disease

0.5 mg vial

PAM-4307-v Amyloid β-Protein (Human, 1-40) [TFA Form](Trifluoroacetate Form) Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val- Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val(M.W. 4329.8) C194H295N53O58SPeptide Deposited in Brain of Alzheimer’s Disease PatientPurity: higher than 95% by HPLC

0.5 mg vial

PAM-4379-v Amyloid β-Protein (Human, 1-40) [HCl Form]Beta amyloid 1-40; Aβ 1-40(Hydrochloride Form)

0.5 mg vial

Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly- Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val(M.W. 4329.8) C194H295N53O58S Peptide Deposited in Brain of Alzheimer’s Disease Patient; Specific Form Easily Convertible to β-StructurePurity: ≥95.0% (HPLC)I. Kaneko, N. Yamada, Y. Sakuraba, M. Kamenosono, and S. Tutumi, J. Neurochem., 65, 2585 (1995). (Original)I. Kaneko and S. Tutumi, J. Neurochem., 68, 438 (1997). (Facile β-Structure Formation)A. Rauk, Chem. Soc. Rev., 38, 2698 (2009). (Review)

PAB-4359-v Amyloid β-Protein (Human, 1-16) Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys (M.W. 1955.0) C84H119N27O28 [131580-10-4] Blocker for Plaque-Induced Microgliosis / Reducer for Brain InflammationD. Giulian, et al., J. Biol. Chem., 273, 29719 (1998). (Original; Pharmacol.)M. Nakamura, et al., Biochemistry, 46, 12737 (2007). (Pharmacol.)

0.5 mg vial

PAM-4309-v Amyloid β-Protein (Human, 25-35)(Trifluoroacetate Form) Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met (M.W. 1060.3) C45H81N13O14S [131602-53-4] Neurotrophic / Neurodegenerative PeptideB.A. Yankner, L.K. Duffy, and D.A. Kirschner, Science, 250, 279 (1990). (Original) L. Meda, et al., Nature, 374, 647 (1995). (Pharmacol.) L. Millucci, L. Ghezzi, G. Bernardini, and A. Santucci, Curr. Protein Pept. Sci., 11, 54 (2010). (Review)

0.5 mg vial

PAB-4367-v [Pyr3]-Amyloid β-Protein (Human, 3-42)(Trifluoroacetate Form)

0.5 mg vial

Pyr-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala (M.W. 4309.9) C196H299N53O55S [183449-57-2] Major Neuritic Plaque Component in Alzheimer’s DiseaseT.C. Saido, et al., Neuron, 14, 457 (1995). (Pharmacol.; Dominant Deposition in Senile Plaques) T. Iwatsubo, et al.i, Am. J. Pathol., 149, 1823 (1996). (Histochem.; Distribution in Brains of Patients) Y.-M. Kuo, et al., Biochem. Biophys. Res. Commun., 237, 188 (1997). (Pharmacol.; Form in Neuritic Plaques and Vascular Amyloid Deposits)


Phone: 502-266-8787 Fax: 502-267-1329



CODE PRODUCT QTY

AMYLOID β PEPTIDES

PAB-4413-s Amyloid β-Protein (40-1)Peptide with Reversed Sequence of Amyloid β-Protein (Human, 1-40)(Trifluoroacetate Form)

0.1 mg vial

Val-Val-Gly-Gly-Val-Met-Leu-Gly-Ile-Ile-Ala-Gly-Lys-Asn-Ser-Gly-Val-Asp-Glu-Ala-Phe-Phe-Val-Leu-Lys-Gln-His-His-Val-Glu-Tyr-Gly-Ser-Asp-His-Arg-Phe-Glu-Ala-Asp (M.W. 4329.8) C194H295N53O58S [144409-99-4] Negative Control Peptide for Amyloid β-Protein (Human, 1-40)

PAB-4420-s Amyloid β-Protein (42-1)Peptide with Reversed Sequence of Amyloid b-Protein (Human, 1-42)(Trifluoroacetate Form)

0.1 mg vial

Ala-Ile-Val-Val-Gly-Gly-Val-Met-Leu-Gly-Ile-Ile-Ala-Gly-Lys-Asn-Ser-Gly-Val-Asp-Glu-Ala-Phe-Phe-Val- Leu-Lys-Gln-His-His-Val-Glu-Tyr-Gly-Ser-Asp-His-Arg-Phe-Glu-Ala-Asp (M.W. 4514.0) C203H311N55O60S [317366-82-8] Negative Control Peptide for Amyloid β-Protein (Human, 1-42)

β-Sheet Breaker Peptide iAβ5p-A1 Available

Amyloid β-protein (Aβ) has been found as insoluble, fibrillar deposits in the brains of Alzheimer’s disease patients. Such deposits are also believed to play a role in diabetes and rheumatoid arthritis. Removal of factors promoting this deposition has been shown to restore normal tissue function implicating viable prevention routes to these diseases. Soto et al. recently reported the design and synthesis of a β-sheet breaker peptide, LPFFD.1 The hydrophobic region of the N-terminal domain of amyloid β-protein (residues 17-20, LVFF) was selected as the model sequence and proline, well known to disrupt β-sheet formation, was incorporated along with a charged residue to aid in solubility. This 5-residue peptide has been found to block amyloid β-fibrillogenesis and is a potential new basis for prevention of amyloidosis in Alzheimer’s patients.

1. C. Soto, E.M. Sigurdsson, L. Morelli, R.A. Kumar, E.M. Castaño, and B. Frangione, Nature Medicine 4, 822 (1998).

PAB-3637-PI Ac-Leu-Pro-N-Me-Phe-Phe-Asp-NH2β-Sheet Breaker Peptide iAb5p-A1(M.W. 692.82) C36H48N6O8 Aβ (1-42) Fibrillogenesis Inhibitor, iAβ5p-A1C. Adessi, et al., J. Biol. Chem., 278, 13905, (2003).

5 mg

PAB-3632-PI Ac-Leu-Pro-Phe-Phe-Asp-NH2β-Sheet Breaker Peptide iAb5p(M.W. 678.89) C35H46N6O8 Aβ (1-42) Fibrillogenesis Inhibitor, iAβ5pC. Soto, E.M. Sigurdsson, L. Morelli, R.A. Kumar, E.M. Castaño, and B. Frangione, Nature Medicine, 4, 822 (1998). B. Permanne, et al., FASEB Journal, 16, 862, (2002).

5 mg

PAB-3631-PI Ac-Lys-N-Me-Leu-Val-N-Me-Phe-Phe-NH2(M.W. 721.95) C39H59N7O6 Membrane Permeable Inhibitor of Aβ (1-40) FibrillogenesisD.J. Gordon, K.L. Sciarretta, and S.C. Meredith, Biochemistry, 40, 8237 (2001). D.J. Gordon, R. Tappe, and S.C. Meredith, J. Pep. Res., 60(1), 37-55 (2002).

1 mg5 mg

PAB-4358-v β-Sheet Breaker Peptide iAβ5Leu-Pro-Phe-Phe-Asp (M.W. 637.72) C33H43N5O8 [182912-74-9] Inhibitor of Amyloid DepositionC. Soto, E.M. Sigurdsson, L. Morelli, R.A. Kumar, E.M. Castano, and B. Frangione, Nat. Med., 4, 822 (1998). (Original, Pharmacol.)

5 mg vial

PAB-3615-PI β-Sheet Breaker Peptide iAβ5 (Bulk)Leu-Pro-Phe-Phe-Asp • AcOH • 4H2O (M.W. 637.74) C33H43N5O8 Inhibitor of Amyloid DepositionC. Soto, E.M. Sigurdsson, L. Morelli, R.A. Kumar, E.M. Castano, and B. Frangione, Nat. Med., 4, 822 (1998). (Original)

5 mg25 mg


Phone: 502-266-8787 Fax: 502-267-1329



CODE PRODUCT QTY

COLIVELIN & HUMANIN

Though the cause of Alzheimer’s Disease (AD) is probably due to multiple factors, increasing evidence indicates accumulation of amyloid β (Aβ) is a major event contributing to neuronal death and disease progression. Recent therapies have focused on use of agents that can decrease amyloid β levels and use of neuroprotective agents. Humanin (PHN-4384-v) is a short polypeptide which was shown to have neuroprotective effects against four representative familial AD (FAD) genes and Aβ peptides.1 Since then, additional humanin derivatives with greater neuroprotective effects have been developed with AGA-(C8R)HNG17 being the most potent.2 Most recently, Chiba and colleagues developed a new hybrid peptide named Colivelin with even greater neuroprotective ability by attaching activity-dependent neurotrophic factor (ADNF) to the C-terminus of AGA-(C8R)HNG17.2 ADNF was first isolated from astrocyte media and was shown to be neuroprotective against AD and non AD related toxic agents.3 ADNF can suppress Aβ toxicity at 100 fM but loses its protective activity at or above nanomolar concentrations.4

Colivelin was shown to be neuroprotective against AD toxicities in vitro and in vivo and can protect against non AD toxicities as well. It is 100x more potent than AGA-(C8R)HNG17 alone and 100,000,000x more potent than humanin. In addition, colivelin does not lose its neuroprotective function at higher concentrations as does ADNF. Colivelin was also shown to block Aβ1-42 and Aβ25-35 impairment of spatial memory and suppress 3-quinuclidinyl benzilate induced memory impairment, suggesting it can pass through the blood-brain barrier. Peptides International offers colivelin as a new exciting tool for the study of Alzheimer’s Disease and possibly other neurodegenerative diseases since most recent findings indicate humanin may also offer neuroprotection against stroke.5

1. Y. Hashimoto, et al., Proc. Natl. Acad. Sci. USA, 98, 6336 (2001).2. T. Chiba, et al., J. Neuroscience, 25, 10252 (2005).3. D.E. Brenneman and I. Gozes, J. Clin. Invest., 97, 2299 (1996).

4. D.E. Brenneman, et al., J. Pharmacol. Exp. Ther., 285, 619 (1998).5. X. Xu, et al., Society for Neuroscience 35th Annual Meeting, (2005).

PHN-3901-PI

ColivelinH-Ser-Ala-Leu-Leu-Arg-Ser-Ile-Pro-Ala-Pro-Ala-Gly-Ala-Ser-Arg-Leu-Leu-Leu-Leu-Thr-Gly-Glu-Ile-Asp-Leu-Pro-OH SALLRSIPAPAGASRLLLLTGEIDLP(M.W. 2645.16) C119H206N32O35Neuroprotective Peptide in Alzheimer’s Disease ResearchT. Chiba, et al., J. Neuroscience, 25, 10252 (2005).

0.5 mg1 mg

PHN-4384-v Humanin Endogenous Rescue Factor Abolishing Neuronal Cell Death

0.5 mg vial

PHN-4385-v [Gly14]-Humanin Potent Rescue Factor Abolishing Neuronal Cell Death

0.5 mg vial

ADNF AGA-(C8R)HNG17 SALLRSIPA PAGASRLLLLTGEIDLP


Phone: 502-266-8787 Fax: 502-267-1329



CODE PRODUCT QTY

RELATED INHIBITORS & SUBSTRATES

SFQ-3690-PI H-Arg-Glu(Edans)-Glu-Val-Asn-Leu-Asp-Ala-Glu-Phe-Lys(Dabcyl)-Arg-OH (M.W. 2005.26) C91H129N25O25S Fluorescence-Quenching Substrate for Memapsin 2 (β-Secretase)J. Ermolieff, J.A. Loy, G. Koelsch, and J. Tang, Biochemistry, 39, 12450 (2000). (substrate termed FS-1 this paper)

1 mg

SMO-3212-v MOCAc-Ser-Glu-Val-Asn-Leu-Asp-Ala-Glu-Phe-Arg-Lys(Dnp)-Arg-Arg-NH2 [MOCAc-SEVNLDAEFRK(Dnp)RR-NH2](7-Methoxycoumarin-4-yl)acetyl-L-Seryl-L-Glutamyl-L-Valyl-L-Asparaginyl-L-Leucyl-L-Aspartyl-L-Alanyl-L- Glutamyl-L-Phenylalanyl-L-Arginyl-Nε-(2,4-Dinitrophenyl)-L-Lysyl-L-Arginyl-L-Arginine Amide(M.W. 2001.1) C86H125N27O29Fluorescence-Quenching Substrate Flanking β-Cleavage Site of Swedish-Type Amyloid Precursor ProteinFibrosis)

T. Hiratsuka, et al., Nephron, 85, 34 (2000). (Pharmacol.)

1 mg vial

IBS-4378-v Lys-Thr-Glu-Glu-Ile-Ser-Glu-Val-Asn-Sta-Val-Ala-Glu-Phe Sta: (3S,4S)-Statine(M.W. 1651.80 ) C73H118N16O27Synthetic ProductInhibitor for β-Secretase

1 mg vial

γ−SECRETASE INHIBITORS & SUBSTRATESSFQ-3217-v Nma-Gly-Gly-Val-Val-Ile-Ala-Thr-Val-Lys(Dnp)-D-Arg-D-Arg-D-Arg-NH2

(Trifluoroacetate Form)Fluorescence-Quenching Substrate for γ-Secretase

1 mg vial

IGS-4394-v L-685,458[(2R,4R,5S)-2-Benzyl-5-(t-Butyloxycarbonylamino)-4-Hydroxy-6-Phenylhexanoyl]-L-Leucyl-L-Phenylalanine AmideSynthetic ProductInhibitor for γ-Secretase

1 mg vial

IGS-3219-v (3,5-Difluorophenylacetyl)-Ala-Phg-OtBuDAPT(3,5-Difluorophenylacetyl)-L-Alanyl-L-Phenylglycine t-butyl esterSynthetic ProductInhibitor for γ-Secretase

5 mg vial

IGS-3641-PI (3,5-Difluorophenylacetyl)-Ala-Phg-OtBuN-[N-(3,5-Difluorophenacetyl)-l-alanyl)]-l-phenylglycine t-butyl ester (M.W. 432.47) C23H26N2O4F2 Inhibitor for γ-SecretaseH.F. Dovey,et al., J. Neurochem., 76, 173 (2001). (Original; Functional γ-Secretase Inhibitor in Brain) A.Y. Kornilova, C. Das, and M.S. Wolfe, J. Biol. Chem., 278, 16470 (2003). (Comparison of in Cells and Cell-Free Activity)

10 mg

Presenilin 1: GSK-3β Target

Glycogen synthase kinase 3 (GSK-3β) is a multifunctional serine/threonine kinase found in all eukaryotes that regulates numerous cell processes. GSK-3β selectively phosphorylates the hydrophilic loop domain of presenilin 1 at the Ser353 and Ser357 and sites. While researchers believe there is a link between the presenilin 1 (PS1) gene and early onset familial Alzheimer’s disease, its role remains unclear. Recently, Kischenbaum and coworkers reported Presenilin 1 (PS1) (SPR-3629-PI) and its mutant (SPR-3630-PI) to be useful tools to separate PS1 function from β-catenin signaling events. While PS1’s association with βcatenin remains controversial, the substitution of one or both serines reduces PS1’s ability to associate with β-catenin. These Alzheimer’s disease related products, presenilin 1 (349-361) and its negative control, are available from Peptides International.F. Kirschenbaum, S.-C Hsu, B. Cordell, and J.V. McCarthy, J. Biol. Chem., 276, 7366-7375 (2000).

SPR-3629-PI Presenilin 1 (349-361)H-Gly-Pro-His-Arg-Ser-Thr-Pro-Glu-Ser-Arg-Ala-Ala-Val-OH(M.W. 1364.5) C56H93N21O19Glycogen Synthase Kinase-3β (GSK-3β) Substrate

1 mg

SPR-3630-PI [Ala353,357]-Presenilin 1 (349-361) H-Gly-Pro-His-Arg-Ala-Thr-Pro-Glu-Ala-Arg-Ala-Ala-Val-OHNegative Control of Glycogen Synthase Kinase-3β Substrate

1 mg


Phone: 502-266-8787 Fax: 502-267-1329



CODE PRODUCT QTY

AMYLOID β-PROTEIN ANTISERA

NAP-14307-v Amyloid β-Protein (Human, 1-40) Antiserum(Rabbit)Antiserum: lyophilized from 0.001 M Phosphate Buffer (pH 7.0) Immunogen: Amyloid β-Protein (Human, 1-40) (Carrier-free) Cross-reactions were not observed at higher doses Specificity: Amyloid β-Protein (Human, 1-40) 100%(1-10 nmol/ml) against the following peptides: Amyloid β-Protein (Human, 1-25) 100% CRF (Human) Amyloid β-Protein (Human, 1-15 Amide) <1% BNP-32 (Human) Amyloid β-Protein (Human, 1-16) <1% Endothelin-1 (Human) Amyloid β-Protein (Human, 26-40) 0% Secretin (Human) Amyloid β-Protein (Human, 17-25) 0% Substance P Amyloid β-Protein (Human, 24-35) 0%

Sensitivity*: IC50 = 0.60 pmol/ml (Antiserum Dilution: x 20,000)* All sensitivity data are measured by enzyme immu-noassay using β-d-galactosidase as a label.

50 μl vial

NAB-14359-v β-Protein (Human, 1-16) AntiserumAmyloid β-Protein N-Terminal Specific Antiserum (Rabbit)Antiserum: lyophilized from 0.001 M Phosphate Buffer (pH 7.0) Immunogen: Amyloid β-Protein (Human, 1-16)-KLH (KLH: Keyhole Limpet Hemocyanin) Reactivity: Amyloid β-Protein (Human, 1-16) + Amyloid β-Protein (Human, 1-40) + Amyloid β-Protein (Human, 1-42) +

Abs

orba

nce

at 4

15 n

m

Serum Dilution

1

0.75

0.5

0.25

0

10000 100000

14359

Antiserum

Normal Serum

Amyloid β Protein (Human, 1-16) Antiserum Dilution CurveAmyloid β Protein (Human, 1-16) Antiserum Dilution Curve

50 μl vial

NAB-14356-v Amyloid β-Protein (Human, 34-40) AntiserumAmyloid β-Protein (1-40) Specific Antiserum (Rabbit) Antiserum: lyophilized from 0.001 M Phosphate Buffer (pH 7.0) Immunogen: Amyloid β-Protein (Human, 34-40)-KLH (KLH: Keyhole Limpet Hemocyanin) Reactivity: Amyloid β-Protein (Human, 1-40) + Amyloid β-Protein (Human, 1-16) - Amyloid β-Protein (Human, 1-42) -

Abs

orba

nce

at 4

15 n

m

Serum Dilution

1

0.75

0.5

0.25

0

10000 100000

14356

Antiserum

Normal Serum


50 µl vial

NAB-14357-v Amyloid β-Protein (Human, 37-42) AntiserumAmyloid β-Protein (1-42) Specific Antiserum (Rabbit) Antiserum: lyophilized from 0.001 M Phosphate Buffer (pH 7.0) Immunogen: Amyloid β-Protein (Human, 37-42)-KLH (KLH: Keyhole Limpet Hemocyanin) Reactivity: Amyloid β-Protein (Human, 1-42) + Amyloid β-Protein (Human, 1-40) - Amyloid β-Protein (Human, 1-16) -

Abs

orba

nce

at 4

15 n

m

Serum Dilution

1

0.75

0.5

0.25

0

10000 100000

14357

Antiserum

Normal Serum


50 µl vial

NAB-14414-v Amyloid β-Protein (Human, 37-43) AntiserumAmyloid β-Protein (1-43) Specific Antiserum (Rabbit)Antiserum: lyophilized from 0.001 M Phosphate Buffer (pH 7.0) Immunogen: Amyloid β-Protein (Human, 37-43)-KLH (KLH: Keyhole Limpet Hemocyanin) Reactivity: Amyloid β-Protein (Human, 1-43) + Amyloid β-Protein (Human, 1-42) - Amyloid β-Protein (Human, 1-40) - Amyloid β-Protein (Human, 1-16) -

Abs

orba

nce

at 4

15 n

m

Serum Dilution

1.8 1.6

1.4

1.2 1.0 0.8 0.6 0.4 0.2 0.0

10000 100000

Antiserum

Normal Serum

14414


50 µl vial


Phone: 502-266-8787 Fax: 502-267-1329



Excellence Compounded.

Peptides International, Inc.11621 Electron DriveLouisville, KY 40299 USAPhone: +1-502-266-8787 Phone: +1-800-777-4779 Fax: +1- 502-267-1329Email: [email protected]: WWW.PEPNET.COM

CATALOG PRODUCTS• RGD Platform• ProTx-II & Other Toxins• Biologically Active Peptides• Substrates & Inhibitors• dPEGs and LinkersFull list @ PEPNET.COM

CUSTOM CHEMISTRY SERVICESMade in USA• Design Consultation• Chemistry Development• Process Scale-up• Pilot-Scale Synthesis• Solution & Solid Phase• SubstratesbyDesignTM

TM

Key literature citations and patents referring to Peptides International products and services

EXCELLENCE COMPOUNDED• High Purity, Quality and Value• StrictConfidentiality• Friendly Service• Proactive Project Management

PEPNET.

neuroscience research peptides · neuroscience research peptides alzheimer’s disease quick...

Documents