1. GPCR/G Protein
  2. GLP Receptor
  3. GLP-1R/GIPR agonist-1 (soduim)

GLP-1R/GIPR agonist-1 sodium is a dual GLP-1/GIP receptor agonist, with an EC50 of 0.57 nM for GLP-1R and an EC50 of 0.75 nM for GIPR. GLP-1R/GIPR agonist-1 sodium reduces food intake, inhibits weight gain, repairs islet damage, improves glucose tolerance, regulates serum lipid and liver enzyme levels, ameliorates hepatic vacuolization, reduces hepatic fat accumulation, delays the progression of hepatic fibrosis, and exhibits long-lasting hypoglycemic activity. GLP-1R/GIPR agonist-1 sodium can be used in research related to type 2 diabetes, obesity, and non-alcoholic steatohepatitis.

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GLP-1R/GIPR agonist-1 (soduim)

GLP-1R/GIPR agonist-1 (soduim) Chemical Structure

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Description

GLP-1R/GIPR agonist-1 sodium is a dual GLP-1/GIP receptor agonist, with an EC50 of 0.57 nM for GLP-1R and an EC50 of 0.75 nM for GIPR. GLP-1R/GIPR agonist-1 sodium reduces food intake, inhibits weight gain, repairs islet damage, improves glucose tolerance, regulates serum lipid and liver enzyme levels, ameliorates hepatic vacuolization, reduces hepatic fat accumulation, delays the progression of hepatic fibrosis, and exhibits long-lasting hypoglycemic activity. GLP-1R/GIPR agonist-1 sodium can be used in research related to type 2 diabetes, obesity, and non-alcoholic steatohepatitis[1].

IC50 & Target

EC50: 0.57 nM (GLP-1R), 0.75 nM (GIPR)

In Vitro

GLP-1R/GIPR agonist-1 sodium (CY-5) is a dual GLP-1R/GIPR agonist without GCGR activity, with an EC50 of 0.57 nM for activating GLP-1R and an EC50 of 0.75 nM for activating GIPR in overexpressed HEK-293 cells[1].

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

In Vivo

GLP-1R/GIPR agonist-1 sodium (30 nM/kg, i.p.; single dose) exerts long-lasting hypoglycemic activity in normal ICR mice, with a duration of action comparable to that of Semaglutide (HY-114118)[1].
GLP-1R/GIPR agonist-1 sodium (30 nM/kg; i.p.; single dose '; daily administration; 32 days (chronic)) achieves acute glycemic stabilization effects comparable to those of Semaglutide in type 2 diabetic mice, and chronic administration significantly reduces food/water intake, suppresses body weight gain, and repairs islet damage[1].
GLP-1R/GIPR agonist-1 sodium (30 nM/kg; i.p.; daily; for 4 consecutive weeks (chronic); single administration ') exerts potent acute appetite-suppressive effects in DIO mice, and also reduces long-term food/water intake, decreases body weight gain, and achieves stable blood glucose control[1].
GLP-1R/GIPR agonist-1 sodium (30 nM/kg; i.p.; single dose) effectively promotes insulin secretion and stabilizes blood glucose in normal SD rats[1].
GLP-1R/GIPR agonist-1 sodium (30 nM/kg; s.c.; single administration) exerts hypoglycemic activity for 34 h in non-fasted ob/ob mice and significantly reduces their body weight[1].
GLP-1R/GIPR agonist-1 sodium (30 nM/kg; i.p.; daily; for 4 consecutive weeks) significantly improves lipid metabolism, reduces liver enzyme levels, and prevents liver injury in NASH mice[1].

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

Animal Model: ICR mice (male, 10 weeks old, 18-22 g)[1]
Dosage: 30 nM/kg
Administration: i.p.; single dose
Result: Exhibited hypoglycemic efficacy duration equivalent to semaglutide.
Maintained blood glucose stabilization through repeated glucose tolerance testing cycles.
Animal Model: ICR mice (male, 10 weeks old, 18-22 g, intraperitoneal injection of 40 mg/kg STZ (HY-13753) followed by 1 week of feeding, fasting blood glucose >11.1 mmol/L, random blood glucose >16.7 mmol/L)[1]
Dosage: 30 nM/kg
Administration: i.p.; single dose (acute testing); daily; 32 days (chronic testing)
Result: Achieved blood glucose stabilization time and glucose reduction percentage equivalent to semaglutide in acute testing.
Suppressed daily and cumulative food/water intake to levels equivalent to semaglutide in chronic treatment.
Significantly inhibited body weight gain (with better weight reduction than CY-16).
Reduced pancreatic islet inflammation, preserved islet cell structure, and repaired islet damage in chronic treatment.
Animal Model: C57BL/6 mice (male, 10 weeks old, 18-22 g, fed high-fat diet for 8 weeks, body weight >20% more than normal diet-fed controls)[1]
Dosage: 30 nM/kg
Administration: i.p.; daily; 4 weeks (chronic testing); single dose (acute appetite suppression testing)
Result: Suppressed cumulative food/water intake to levels equivalent to semaglutide in chronic treatment.
Inhibited body weight gain more effectively than E1 in chronic treatment.
Maintained stable fasting blood glucose levels in chronic treatment.
Resulted in near-zero food intake in the first 8 h post-administration in acute treatment, with cumulative food intake equivalent to semaglutide.
Preserved pancreatic islet structure in chronic treatment.
Animal Model: SD rats (male, 5-6 weeks old, 180-220 g)[1]
Dosage: 30 nM/kg
Administration: i.p.; single dose
Result: Significantly promoted insulin secretion (with insulin AUC0-180ₘᵢₙ equivalent to semaglutide).
Reduced blood glucose AUC0-180ₘᵢₙ compared to saline controls.
Stabilized blood glucose levels post-administration, with no sharp peak observed in the saline group.
Animal Model: B6.v-Lepob/J (ob/ob) mice (6-7 weeks old, half male/half female)[1]
Dosage: 30 nM/kg
Administration: s.c.; single dose
Result: Significantly decreased blood glucose starting 2 h post-administration, with hypoglycemic duration lasting 34 h.
Reduced body weight by 2.0 g at 24 h, 0.9 g at 48 h, and 0.1 g at 72 h post-administration, which was significantly lower than the control group and equivalent to semaglutide.
Animal Model: C57BL/6 mice (male, fed NASH-inducing diet [40% fat, 40% carbohydrates, 2% cholesterol] for 8 weeks)[1]
Dosage: 30 nM/kg
Administration: i.p.; daily; 4 weeks
Result: Significantly reduced serum TG, TC, LDL-C, AST, and ALT levels compared to saline controls.
Significantly increased serum HDL-C levels compared to saline controls.
Showed significant improvement in hepatocyte inflammation, reduced lipid droplets, and improved liver vacuolation compared to the saline group, with better liver protection than semaglutide.
Molecular Weight

4861.38 (free base)

Formula

C220H334N55O69.xNa

Appearance

Solid

Color

White to off-white

Sequence

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

Sequence Shortening

H-{Aib}-QGTFTSDYSK-{Aib}-LDKRAA-K(AEEA-AEEA-gammaGlu-C18 diacid)-DFVEWLKNGGPSSGAPPPS-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 : ≥ 100 mg/mL

*"≥" means soluble, but saturation unknown.

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Help & FAQs
  • 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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Product Name:
GLP-1R/GIPR agonist-1 (soduim)
Cat. No.:
HY-P10302A
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