NN1213
Based on 1 Customer Validation
NN1213, a long-acting human amylin peptide analog, is a selective Amylin receptor agonist with EC50 values of 0.177 and 0.262 nM for hAMY3R and rAMY3R, respectively. NN1213 significantly reduces food intake and fat mass. NN1213 can reduce body weightin diet-induced obese rats. NN1213 can be used for the research of obesity.
For research use only. We do not sell to patients.
- Purity : 99.03%
- Formula: C198H316N56O63S2
- Molecular Weight:4553.10
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
NN1213 shows EC50 values of 0.177 and 0.262 nM for hAMY3R and rAMY3R[1].
NN1213 shows binding affinity values of 0.561 and 0.29 nM for hAMY3R and rAMY3R[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
NN1213 (3-100 nmol/kg; s.c.; single dose) produces a dose-dependent, long-duration reduction in food intake in rats[1].
NN1213 (3-300 nmol/kg; s.c.; single dose) produces a dose-dependent, long-duration reduction in food intake in beagle dogs[1].
NN1213 (10 nmol/kg; s.c.; daily; 17 days) decreases body weight and food intake in diet-induced obese rats[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Rat (diet-induced obese, fed high-energy diet)[1]
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Dosage:0.7 nmol/kg (3 µg/kg); 2.2 nmol/kg (10 µg/kg); 6.6 nmol/kg (30 µg/kg); 22 nmol/kg (100 µg/kg)
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Administration:s.c.; daily; 21 days
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Result:Transiently reduced food intake, with maximal suppression during days 1-2; by day 15, food intake was close to vehicle control levels but still slightly reduced.
Produced dose-dependent body weight loss: the 0.7 nmol/kg group lost 4.7% of baseline body weight, while the 2.2, 6.6, and 22 nmol/kg groups lost 8.7-9.3% of baseline body weight.
Over 21 days, the 0.7 nmol/kg group lost 32.0 ± 3.6 g, and the 22 nmol/kg group lost 69.6 ± 7.5 g (equivalent to 90.7% of initial body weight).
Confirmed via magnetic resonance imaging that body weight loss was primarily driven by a dose-dependent reduction in fat mass, with minimal effects on lean mass.
Chemical Information
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Appearance Solid
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Molecular Weight 4553.10
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Formula C198H316N56O63S2
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Color White to off-white
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Sequence
{Lys(γGlu-γGlu-C20 diacid)}-Cys-Asn-Thr-Ala-Thr-Cys-Ala-Thr-Gln-Arg-Leu-Ala-Asp-Phe-Leu-Arg-His-Ser-Ser-Pro-Asn-Phe-Gly-Ala-Ile-Pro-Ser-Ser-Thr-Asn-Val-Gly-Ser-Arg-Thr-Tyr-NH2 (disulfide bridge:Cys2-Cys7)
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Sequence Shortening
{Lys(γGlu-γGlu-C20 diacid)}-CNTATCATQRLADFLRHSSPNFGAIPSSTNVGSRTY-NH2 (disulfide bridge:Cys2-Cys7)
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Protocols
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
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Data Sheet (265 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
NN1213 Related Classifications
HY-P11245 Related Classifications
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