Zenagamtide sodium can activate GLP-1, amylin, and calcitonin receptors in human, mouse, and rat cellular systems[1]. Zenagamtide sodium (10-fold to 3-fold serial dilutions; 30 minutes to 3 hours) can effectively activate GLP-1R, AMY3(a)R, and CTR in human, mouse, and rat cells, with EC50 values ranging from 8.4 × 10⁻¹³ M to 7.8 × 10⁻¹¹ M[2]. Zenagamtide sodium (10-fold serial dilutions; 30 minutes) can effectively activate human AMY1(a)R, AMY2(a)R, AMY3(a)R, and CTR(a), with EC50 values ranging from 1.30 × 10⁻¹² M to 1.72 × 10⁻¹¹ M[2].

Subcutaneous injection of Zenagamtide (sodium) (subchronic and chronic administration) in diet-induced obese rats reduced total energy intake and body weight, and improved insulin sensitivity and metabolic health indicators [1]. Zenagamtide (sodium) (10 nmol/kg; subcutaneous; single dose) reduced cumulative food intake by 50% in normal-weight male Sprague Dawley rats over 48 hours [2]. Zenagamtide (sodium) (2-10 nmol/kg; subcutaneous; twice daily; for 21 days) reduced total food intake by 23-30% in male DIO C57Bl/6J mice and induced a carrier-corrected weight loss of 15.8-21.3% in a dose-dependent manner [2]. Zenagamtide (sodium) (1→3→10 nmol/kg; subcutaneous; once daily; for 21 days) reduced total energy intake by 47.4% in male DIO Sprague Dawley rats and reduced body weight (carrier-corrected) by 18.3% while maintaining total energy expenditure [2]. Zenagamtide (sodium) (1→3→10 nmol/kg; subcutaneous injection; once daily; for 35 days) reduced HOMA-IR by 47% in male DIO Sprague Dawley rats and increased steady-state glucose infusion rate by three times, indicating improved insulin sensitivity [2]. Zenagamtide (sodium) (10-30 nmol/kg; subcutaneous injection; twice daily; for 12 weeks) reduced plasma liver enzyme levels, improved MASLD activity scores in 55.6-64.7% of mice, and reduced biopsy-confirmed liver inflammation and fibrosis markers in male GAN DIO-MASH C57BL/6JRj mice [2]. Fluorescently labeled Zenagamtide (sodium) (100 nmol/kg; intravenous injection; single dose) reached key brain regions involved in energy uptake regulation in male C57BL/6J mice, including periventricular organs and hypothalamus/hindbrain regions [2].

Animal/Disease Models:C57Bl/6J (male, 25 weeks old, weight 39-56 g, diet-induced obesity) [2]
Doses: 2 nmol/kg; 10 nmol/kg
Route of Administration: Subcutaneous injection; twice daily; for 21 days
Experimental Results: Total food intake was reduced by 23% in the 2 nmol/kg dose group and by 30% in the 10 nmol/kg dose group. The 2 nmol/kg and 10 nmol/kg dose groups reduced the carrier-corrected body weight by 15.8% and 21.3%, respectively, with significant differences between the two target reagent dose groups.

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Animal/Disease Models:Sprague Dawley mice (male, approximately 750 g, diet-induced obesity)[2]
Doses: 1 nmol/kg (day 1); 3 nmol/kg (day 2); 10 nmol/kg (days 3–21)
Route of Administration: Subcutaneous injection; once daily for 21 days
Experimental Results: After 21 days, body weight was reduced by 18.3% compared to the vector control group. Total energy intake was reduced by 47.4% compared to the vector control group. There was no significant difference in total energy expenditure compared to the vector group, while the total energy expenditure of the weight-matched group with restricted calorie intake was 13.6% lower than that of the target reagent group.

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Animal/Disease Models:Sprague Dawley mice (male, diet-induced obesity) [2]
Doses: 1 nmol/kg (day 1); 3 nmol/kg (day 2); 10 nmol/kg (days 3-35)
Route of Administration: Subcutaneous injection; once daily for 35 days
Experimental Results: Baseline fasting blood glucose decreased by 7% (carrier group: 121.1 ± 3.0 mg/dL vs. target reagent group: 112 ± 2.1 mg/dL; p < 0.05). Baseline fasting plasma insulin decreased by 42% (carrier group: 77.0 ± 6.7 µU/mL vs. target reagent group: 44.8 ± 4.0 µU/mL; p < 0.001). HOMA-IR decreased by 47% (carrier group: 23.4 ± 2.3 vs. target group: 12.5 ± 1.2; p < 0.001). During the clamp test, the glucose infusion rate required to maintain normal blood glucose was three times that of the control group (mean steady-state glucose infusion rate: carrier group: 5.53 ± 1.17 mg/kg/min vs. target group: 16.4 ± 2.10 mg/kg/min; p < 0.001). Compared with the carrier control group, glucose uptake measured by the tracer increased by 37% (carrier group: 15.7 ± 1.51 mg/kg/min vs. target group: 24.8 ± 1.33 mg/kg/min; p < 0.001), while there was no difference in hepatic glucose production between the two groups.

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Animal/Disease Models:C57BL/6JRj (male, Gubra-Amylin NASH diet-induced obesity-related fatty liver disease, fibrosis stage F2-3, steatosis score 3, inflammation score ≥2) [2]
Doses: 10 nmol/kg (titration: 0.5→1→2→6→10 nmol/kg); 30 nmol/kg (titration: 0.5→1→2→6→12→30 nmol/kg)
Route of Administration: Subcutaneous injection; twice daily; 12 weeks
Experimental Results: Both doses significantly reduced plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels (p < 0.001 compared to the vector). In mice treated with 10 nmol/kg, 55.6% showed an improvement of ≥2 points in MASLD activity score; in mice treated with 30 nmol/kg, 64.7% showed an improvement of ≥2 points in MASLD activity score (p < 0.001 compared to the vector group, where the improvement rate was 0%). Both doses significantly reduced the intensity of hepatic galactolectin-3 staining (an inflammatory marker) (p < 0.05 in the 10 nmol/kg group and p < 0.01 in the 30 nmol/kg group, compared to the vector group). Both doses significantly reduced the intensity of hepatic α-smooth muscle actin staining (a fibrosis marker) (p < 0.001 compared to the vector group). The proportion of lipid droplets in hepatocytes decreased to 42.2% and 29.4% in the 10 nmol/kg and 30 nmol/kg groups, respectively (p < 0.001 compared to 77.9% in the vector group).

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Animal/Disease Models:C57BL/6J (male, 25 g) [2]
Doses: 100 nmol/kg
Route of Administration: Intravenous injection; single dose
Experimental Results: Fluorescent signals were detected in the periventricular organs (posterior region, median eminence, lamina terminalis vascularis, subfornular organs) and the blood-brain barrier protected areas (arctic nucleus, solitary nucleus, dorsal motor nucleus of the vagus nerve) at 2 and 6 hours after administration. The signal intensity was highest in the periventricular organs at 2 hours after administration.

[1]. 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]. 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.

[3]. 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.

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

C343H550N94O116.XNA

7846.60 (free base)

Zenagamtide; 3005889-81-3

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-NH2H-Aib-EGTFTSDVSSYLEEQAAREFIAWLVRGR-{Lys(AEEA-AEEA-γGlu-C18 diacid)}-GGGGEASELSTAALGRLSAELHELATLPRTETGSGSP-NH2

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

White to off-white solid

Amycretin sodium; NN 9487 sodium

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: 请将本产品存放在密封保护的环境中，避免受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~10 mg/mL (with sonication)
DMSO : ~2 mg/mL (with sonication)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)