| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| Other Sizes |
| Targets |
Human GIP receptor (hGIPR). Human GIP(3-30), amide TFA acts as a high-affinity antagonist of the human GIP receptor in vitro, blocking GIP-induced signaling. The GIP receptor is a G protein-coupled receptor (GPCR) that is expressed in pancreatic β-cells, adipose tissue, bone, and the central nervous system. Upon activation by GIP(1-42), the receptor couples to Gs proteins, leading to activation of adenylyl cyclase, increased cAMP levels, and activation of protein kinase A (PKA) and Epac. This signaling pathway stimulates insulin secretion, promotes β-cell proliferation and survival, and regulates lipid metabolism. By competitively binding to the GIP receptor, human GIP(3-30), amide TFA blocks GIP-mediated signaling, thereby inhibiting GIP-stimulated insulin secretion and other GIP-dependent effects.
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| ln Vitro |
GIP(3-30)NH2 is a potent competitive antagonist of the GIP receptor and effectively inhibits GIP-mediated insulin, glucagon, and somatostatin release. In vitro, human GIP(3-30), amide TFA acts as a high-affinity antagonist of the human GIP receptor, blocking GIP-induced signaling. It inhibits GIP-stimulated insulin secretion in pancreatic β-cells and cAMP production in GIP receptor-expressing cells. By blocking GIP receptor signaling, the peptide also inhibits GIP-mediated effects on adipocytes, including lipogenesis and fat storage. Detailed IC50 or Ki values are not provided in the available literature, but the compound is described as a high-affinity antagonist.
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| ln Vivo |
Human GIP(3-30), amide TFA has potential anti-obesity and anti-diabetic effects by blocking GIP receptor signaling. GIP plays a role in glucose homeostasis, insulin secretion, and energy balance. In obesity, GIP levels are elevated, and GIP receptor signaling promotes fat storage and adiposity. By blocking GIP receptor signaling, GIP(3-30)NH2 may reduce fat accumulation and improve glucose tolerance. In animal models of obesity and diabetes, GIP receptor antagonists have been shown to improve glucose tolerance, reduce body weight, and ameliorate insulin resistance. The peptide is used in research to investigate the role of GIP in metabolic disorders such as diabetes and obesity.
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| Enzyme Assay |
Receptor binding assays are performed using radiolabeled GIP (e.g., 125I-GIP) incubated with membranes expressing the human GIP receptor in the presence of varying concentrations of human GIP(3-30), amide TFA. Bound radioactivity is separated from free radioligand by filtration or centrifugation, and the inhibition of specific binding is calculated. IC50 or Ki values are determined by fitting competition binding data to a sigmoidal dose-response curve. The high-affinity binding of the antagonist to the GIP receptor confirms its ability to compete with the natural ligand for receptor occupancy.
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| Cell Assay |
cAMP accumulation assays are performed using cells expressing the human GIP receptor (e.g., HEK293 or CHO cells stably transfected with hGIPR) treated with human GIP(3-30), amide TFA followed by GIP(1-42) stimulation. Intracellular cAMP levels are measured via ELISA or FRET-based methods (e.g., using a cAMP biosensor or competitive immunoassay). The ability of the antagonist to inhibit GIP-stimulated cAMP production demonstrates its functional antagonism at the receptor level. β-arrestin recruitment assays can also be performed to assess the effects of the antagonist on GIP-induced β-arrestin signaling.
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| Animal Protocol |
Animal models of obesity and diabetes (e.g., diet-induced obese mice, db/db mice, high-fat diet-fed mice) are administered human GIP(3-30), amide TFA via subcutaneous or intraperitoneal routes. Glucose tolerance tests (OGTT) are performed to assess the effects of the antagonist on glucose handling. Insulin levels are measured to evaluate the effects on insulin secretion. Body weight and food intake are monitored to assess the effects on energy balance. The peptide is used in research to investigate the role of GIP in metabolic disorders.
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| ADME/Pharmacokinetics |
Peptide antagonists such as human GIP(3-30), amide TFA typically have short half-lives due to rapid renal clearance and proteolytic degradation. GIP(3-30)NH2 is a naturally occurring metabolite of GIP, and its half-life is limited by DPP-4 cleavage and renal clearance. Pharmacokinetic parameters are evaluated in rodents; metabolic stability may be improved by modifications to resist DPP-4 cleavage. The peptide is typically administered via parenteral routes (subcutaneous, intraperitoneal, intravenous) for in vivo studies. Detailed PK data specific to human GIP(3-30), amide TFA are not extensively reported in the available literature.
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| Toxicity/Toxicokinetics |
Peptide-based GIP receptor antagonists are generally well-tolerated at therapeutic doses. Potential toxicities may include gastrointestinal effects and hypoglycemia due to GIP signaling blockade. GIP plays a role in glucose-dependent insulin secretion, and its blockade could theoretically impair glucose-stimulated insulin release, leading to glucose intolerance or hyperglycemia in certain contexts. However, in obesity and diabetes models, GIP receptor antagonists have shown beneficial effects, suggesting a favorable risk-benefit profile. Standard toxicology studies are required for therapeutic development. As a research compound, detailed toxicology data are not publicly available.
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| References | |
| Additional Infomation |
Human GIP(3-30), amide TFA is a research-grade peptide antagonist for metabolic research. It is a synthetic peptide corresponding to amino acids 3-30 of human GIP with C-terminal amidation, supplied as a TFA salt. It is a potent competitive antagonist of the GIP receptor and effectively inhibits GIP-mediated insulin, glucagon, and somatostatin release. Synonyms: GIP(3-30)NH2. For research use only, not for human therapeutic use.
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| Molecular Formula |
C150H226N38O44S.XC2HF3O2
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| Molecular Weight |
3297.69 (free base)
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| Appearance |
White to off-white solid powder
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO :~100 mg/mL (with sonication)
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| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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