| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
Human GIP receptor (hGIPR). (Pro3) GIP, human TFA is a full agonist of the human GIP receptor. 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, 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, regulates lipid metabolism, and has effects on bone turnover. (Pro3) GIP activates the GIP receptor with high potency, as demonstrated by its low Ki/Kd value of 0.90 nM.
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| ln Vitro |
(Pro3) GIP, human TFA is a full agonist of the human GIP receptor with high binding affinity (Ki/Kd = 0.90 nM). It activates GIPR signaling pathways, including cAMP production and insulin secretion. In vitro, (Pro3) GIP stimulates cAMP accumulation in GIP receptor-expressing cells, indicating potent receptor activation. The peptide is more stable than native GIP due to the Pro3 substitution, which prevents DPP-4-mediated cleavage at the N-terminus. This stability makes (Pro3) GIP a valuable tool for studying the physiological and pharmacological effects of GIP receptor activation without the rapid degradation that limits the utility of native GIP.
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| ln Vivo |
(Pro3) GIP, human TFA has potential therapeutic applications in obesity and type 2 diabetes by activating GIP receptor signaling. GIP plays a crucial role in glucose homeostasis, insulin secretion, and energy balance. In obesity and type 2 diabetes, the incretin effect is impaired, and GIP receptor signaling may be altered. By activating the GIP receptor, (Pro3) GIP can stimulate glucose-dependent insulin secretion, improve glucose tolerance, and potentially promote β-cell survival and function. Daily (Pro3) GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes. The peptide may also have effects on adipose tissue and bone metabolism.
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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 (Pro3) GIP, human TFA. Bound radioactivity is separated from free radioligand by filtration or centrifugation, and the inhibition of specific binding is calculated. The Ki (inhibition constant) or Kd (dissociation constant) is determined by fitting competition binding data to a sigmoidal dose-response curve. The high binding affinity of (Pro3) GIP (Ki/Kd = 0.90 nM) confirms its potent interaction with the GIP receptor.
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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 (Pro3) GIP, human TFA. Intracellular cAMP levels are measured via ELISA or FRET-based methods (e.g., using a cAMP biosensor or competitive immunoassay). The ability of (Pro3) GIP to stimulate cAMP production in a concentration-dependent manner demonstrates its agonist activity at the receptor. EC50 values are determined from dose-response curves. The peptide's full agonist activity confirms that it activates the receptor to the same maximal extent as native GIP.
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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 (Pro3) GIP, human TFA via subcutaneous or intraperitoneal routes. Glucose tolerance tests (OGTT) are performed to assess the effects of the agonist on glucose handling. Insulin secretion is measured to evaluate the effects on β-cell function. Food intake and body weight are monitored to assess the effects on energy balance. In obesity-related diabetes models, daily (Pro3) GIP administration improves glucose tolerance, ameliorates insulin resistance, and improves islet structure.
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| ADME/Pharmacokinetics |
(Pro3) GIP is engineered for enhanced stability compared to native GIP, with resistance to DPP-4 cleavage. The Pro3 substitution prevents the rapid degradation that limits the half-life of native GIP, resulting in improved pharmacokinetic properties. The peptide is expected to have a longer half-life and improved bioavailability compared to native GIP. Pharmacokinetic parameters (Cmax, Tmax, AUC, t1/2) are evaluated in rodents. The peptide is typically administered via parenteral routes (subcutaneous, intraperitoneal) for in vivo studies.
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| Toxicity/Toxicokinetics |
(Pro3) GIP, human TFA is a peptide GIP receptor agonist with an expected safety profile typical of incretin-based therapies. GLP-1 receptor agonists (another class of incretin-based therapies) have been extensively studied and are generally well-tolerated, with gastrointestinal effects being the most common side effects. GIP receptor agonists may have similar safety considerations. Potential toxicities may include gastrointestinal effects (nausea, vomiting) and hypoglycemia, particularly when used in combination with other glucose-lowering agents. Standard toxicology studies are required for therapeutic development. As a research compound, detailed toxicology data are not publicly available.
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| References |
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| Additional Infomation |
(Pro3) GIP, human TFA is a research-grade GIP receptor agonist for metabolic research. It is a synthetic peptide with proline substitution at position 3 to confer DPP-4 resistance and enhance stability. It is a full agonist of the human GIP receptor with high binding affinity (Ki/Kd = 0.90 nM). Synonyms: (Pro3) Gastric Inhibitory Peptide, human TFA. For research use only, not for human therapeutic use.
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| Molecular Formula |
C226H338N60O64S.XC2HF3O2
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| Molecular Weight |
4951.53 (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)
H2O :≥ 100 mg/mL |
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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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