Zenagamtide sodium (Synonyms: Amycretin sodium; NN 9487 sodium)

Name: Zenagamtide sodium
Brand: MedChemExpress
SKU: HY-P11274A
Rating: 5.0 (1 reviews)

Cat. No.: HY-P11274A Purity: 99.96%: Data Sheet
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Zenagamtide (Amycretin; NN 9487) sodium is an orally active, blood-brain barrier permeable triple agonist that targets GLP-1, amylin (Amylin Receptor) and calcitonin receptor (Calcitonin Receptor). Zenagamtide sodium is a single peptide consisting of 68 amino acids that can target brain regions regulating food intake, significantly suppress appetite and reduce energy intake. Therefore, Zenagamtide sodium improves body weight, waist circumference, glycated hemoglobin and lipid profile, and also alleviates the histological features of metabolic dysfunction-associated steatotic liver disease (MASLD) and enhances insulin sensitivity. Zenagamtide sodium may cause transient increases in heart rate and fluctuations in serum calcium levels, but it is an important compound for the study of overweight, obesity, insulin resistance and related metabolic diseases.

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Zenagamtide sodium Chemical Structure

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1 mg	In-stock	Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

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Description

IC₅₀ & Target

GLP-1^[1]

In Vitro

Zenagamtide sodium activates GLP-1, amylin and calcitonin receptors in cellular systems of humans, mice and rats^[1].
Zenagamtide sodium (10-fold to 3-fold serial dilution; 30 min-3 h) potently activates human, mouse and rat GLP-1R, mouse and rat AMY_{3 (a)}R, as well as mouse and rat CTR, with EC₅₀ values ranging from 8.4×10^-13 M to 7.8×10^-11 M^[2].
Zenagamtide sodium (10-fold serial dilution; 30 min) potently activates human AMY_{1 (a)}R, AMY_{2 (a)}R, AMY_{3 (a)}R, and CTR_(a), with EC₅₀ values ranging from 1.30×10^-12 M to 1.72×10^-11 M^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Parmacokinetics

Species	Dose	Route	C_max	T_max	AUC_0-∞	T_1/2	C₀	CL	V_z
Mice^[2]	0.08 (10 nmol/kg) mg/kg	s.c.	37.7 nM	2.00 h	309 ng·h/mL	3.65 h	/	/	/
Rat^[2]	0.012 (1.5 nmol/kg) mg/kg	i.v.	/	/	94.4 ng·h/mL	5.92 h	19.2 nM	0.0160 L/h/kg	0.137 L/kg
Pig^[2]	0.016 (1.5 nmol/kg) mg/kg	i.v.	/	/	1510 ng·h/mL	54.1 h	44.7 nM	0.00122 L/h/kg	0.0956 L/kg

In Vivo

Zenagamtide (sodium) (s.c.; subchronic; chronic) administered to diet-induced obese rats reduces total energy intake and bodyweight, and improves insulin sensitivity and metabolic health markers^[1].
Zenagamtide (sodium) (10 nmol/kg; s.c.; single dose) reduces 48-hour cumulative food intake by 50% in normal weight male Sprague Dawley rats^[2].
Zenagamtide (sodium) (2-10 nmol/kg; s.c.; twice daily; 21 days) reduces total food intake by 23-30% and induces vehicle-adjusted body weight loss of 15.8-21.3% in a dose-dependent manner in male DIO C57Bl/6J mice^[2].
Zenagamtide (sodium) (1→3→10 nmol/kg; s.c.; once daily; 21 days) reduces total energy intake by 47.4% and induces 18.3% vehicle-adjusted body weight loss while maintaining total energy expenditure in male DIO Sprague Dawley rats^[2].
Zenagamtide (sodium) (1→3→10 nmol/kg; s.c.; once daily; 35 days) reduces HOMA-IR by 47% and increases steady-state glucose infusion rate three-fold, indicating improved insulin sensitivity, in male DIO Sprague Dawley rats^[2].
Zenagamtide (sodium) (10-30 nmol/kg; s.c.; twice daily; 12 weeks) reduces plasma liver enzyme levels, improves MASLD activity scores in 55.6-64.7% of mice, and reduces liver inflammation and fibrosis markers in biopsy-confirmed GAN DIO-MASH male C57BL/6JRj mice^[2].
Fluorescently labelled Zenagamtide (sodium) (100 nmol/kg; i.v.; single dose) reaches key brain regions involved in energy intake regulation, including circumventricular organs and hypothalamic/hindbrain regions, in male C57BL/6J mice^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:	C57Bl/6J (male, 25 weeks old, 39-56 g, diet-induced obese)^[2]
Dosage:	2 nmol/kg; 10 nmol/kg
Administration:	s.c.; twice daily; 21 days
Result:	Reduced total 21-day food intake by 23% with 2 nmol/kg and 30% with 10 nmol/kg. Induced vehicle-adjusted body weight loss of 15.8% with 2 nmol/kg and 21.3% with 10 nmol/kg, with a significant difference between the two target reagent doses.

Animal Model:	Sprague Dawley (male, ~750 g, diet-induced obese)^[2]
Dosage:	1 nmol/kg (day 1); 3 nmol/kg (day 2); 10 nmol/kg (days 3-21)
Administration:	s.c.; once daily; 21 days
Result:	Induced 18.3% vehicle-adjusted body weight loss after 21 days. Reduced total energy intake by 47.4% compared to vehicle control. Showed no significant difference in total energy expenditure compared to vehicle groups, while the calorie-restricted weight-matched group had 13.6% lower total energy expenditure than the target reagent group.

Animal Model:	Sprague Dawley (male, diet-induced obese)^[2]
Dosage:	1 nmol/kg (day 1); 3 nmol/kg (day 2); 10 nmol/kg (days 3-35)
Administration:	s.c.; once daily; 35 days
Result:	Reduced baseline fasting blood glucose by 7% (vehicle: 121.1 ± 3.0 mg/dL vs. target reagent: 112 ± 2.1 mg/dL; p < 0.05). Reduced baseline fasting plasma insulin by 42% (vehicle: 77.0 ± 6.7 µU/mL vs. target reagent: 44.8 ± 4.0 µU/mL; p < 0.001). Reduced HOMA-IR by 47% (vehicle: 23.4 ± 2.3 vs. target reagent: 12.5 ± 1.2; p < 0.001). Required a three-fold higher glucose infusion rate to maintain euglycaemia during clamp (average steady-state GIR: vehicle: 5.53 ± 1.17 mg/kg/min vs. target reagent: 16.4 ± 2.10 mg/kg/min; p < 0.001). Increased tracer-determined glucose uptake by 37% compared to vehicle control (vehicle: 15.7 ± 1.51 mg/kg/min vs. target reagent: 24.8 ± 1.33 mg/kg/min; p < 0.001), while hepatic glucose production did not differ between groups.

Animal Model:	C57BL/6JRj (male, Gubra-Amylin NASH diet-induced obese metabolic dysfunction-associated steatotic liver disease, fibrosis stage F2-3, steatosis score 3, inflammation score ≥2)^[2]
Dosage:	10 nmol/kg (titrated: 0.5→1→2→6→10 nmol/kg); 30 nmol/kg (titrated: 0.5→1→2→6→12→30 nmol/kg)
Administration:	s.c.; twice daily; 12 weeks
Result:	Significantly reduced plasma alanine transaminase (ALT) and aspartate transaminase (AST) levels with both doses (p < 0.001 vs. vehicle). Achieved ≥2-point improvement in MASLD activity score in 55.6% of mice treated with 10 nmol/kg and 64.7% treated with 30 nmol/kg (p < 0.001 vs. vehicle, which had 0% improvement). Significantly reduced liver galectin-3 staining (inflammation marker) with both doses (p < 0.05 for 10 nmol/kg, p < 0.01 for 30 nmol/kg vs. vehicle). Significantly reduced liver α-smooth muscle actin staining (fibrosis marker) with both doses (p < 0.001 vs. vehicle). Reduced hepatocytes with lipid droplets to 42.2% with 10 nmol/kg and 29.4% with 30 nmol/kg (p < 0.001 vs. vehicle's 77.9%).

Animal Model:	C57BL/6J (male, 25 g)^[2]
Dosage:	100 nmol/kg
Administration:	i.v.; single dose
Result:	Detected fluorescent signal in circumventricular organs (area postrema, median eminence, vascular organ of the lamina terminalis, subfornical organ) and blood-brain barrier-protected regions (arcuate hypothalamic nucleus, nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve) at 2 and 6 hours post-dose. Showed highest signal intensity in circumventricular organs at 2 hours post-dose.

Molecular Weight

7846.60 (free base)

Formula

C₃₄₃H₅₅₀N₉₄O₁₁₆.xNa

Appearance

Solid

Color

White to off-white

Sequence

His-Aib-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Val-Ser-Ser-Tyr-Leu-Glu-Glu-Gln-Ala-Ala-Arg-Glu-Phe-Ile-Ala-Trp-Leu-Val-Arg-Gly-Arg-{Lys(AEEA-AEEA-γGlu-C18 diacid)}-Gly-Gly-Gly-Gly-Glu-Ala-Ser-Glu-Leu-Ser-Thr-Ala-Ala-Leu-Gly-Arg-Leu-Ser-Ala-Glu-Leu-His-Glu-Leu-Ala-Thr-Leu-Pro-Arg-Thr-Glu-Thr-Gly-Ser-Gly-Ser-Pro-NH2

Sequence Shortening

H-Aib-EGTFTSDVSSYLEEQAAREFIAWLVRGR-{Lys(AEEA-AEEA-γGlu-C18 diacid)}-GGGGEASELSTAALGRLSAELHELATLPRTETGSGSP-NH2

Shipping

Room temperature in continental US; may vary elsewhere.

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)

Solvent & Solubility

In Vitro:

H₂O : 10 mg/mL (Need ultrasonic)

DMSO : 2 mg/mL (Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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Purity & Documentation

Purity: 99.96%

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Data Sheet (317 KB) SDS (254 KB)

COA (290 KB) RP-HPLC (265 KB) MS (233 KB) Elemental Analysis Report (148 KB)

Handling Instructions (2659 KB)

References

[1]. Dahl K, et al. Amycretin, a novel, unimolecular GLP-1 and amylin receptor agonist administered subcutaneously: results from a phase 1b/2a randomised controlled study[J]. The Lancet, 2025, 406(10499): 149-162.

[2]. Kuhre RE, et al. The effect of amycretin, a unimolecular glucagon-like peptide-1 and amylin receptor agonist, on body weight and metabolic dysfunction in mice and rats. EBioMedicine. 2025;118:105862. [Content Brief]

[3]. Gasiorek A, et al. Safety, tolerability, pharmacokinetics, and pharmacodynamics of the first-in-class GLP-1 and amylin receptor agonist, amycretin: a first-in-human, phase 1, double-blind, randomised, placebo-controlled trial. Lancet. 2025;406(10499):135-148. [Content Brief]

[4]. Khoo B, et al. GLP-1 and amylin receptor multiagonism with amycretin for obesity management[J]. The Lancet, 2025, 406(10499): 104-106.

Zenagamtide sodium Related Classifications

Metabolic Disease

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Do most proteins show cross-species activity?
Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Zenagamtide sodium (Synonyms: Amycretin sodium; NN 9487 sodium)

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