| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 50mg | |||
| 100mg | |||
| 250mg | |||
| Other Sizes |
| ln Vitro |
In STF-cMyc cells, Bax inhibitor peptide V5 (BIP-V5; 0–50 μM) decreased cell mortality, but not in SW620 or NCI-H23 cells. In the G2/M phase, BIPV5 has no discernible impact on cell cycle arrest [1]. The administration of V5 therapy resulted in an increase of almost thrice for the anti-apoptotic proteins Bcl-2 and XIAP and a decrease of over thirty, thirty, and almost fifty percent for the apoptosis-inducing proteins Bax, Bad, and nuclear factor-κB-p65, respectively[2].
1. Inhibition of pancreatic β-cell apoptosis (Reference [2]): Isolated mouse pancreatic islets were treated with Bax inhibitor peptide V5 (1, 5, 10 μM) under apoptotic conditions (high glucose: 25 mM + palmitic acid: 0.5 mM) for 48 hours. Annexin V-FITC/PI staining showed that Bax inhibitor peptide V5 dose-dependently reduced apoptosis rate: 10 μM V5 decreased apoptosis from 45% (vehicle) to 18%. Western blot showed reduced cleaved caspase-3 (by 60% at 10 μM) and cytochrome c release from mitochondria (by 55% at 10 μM) [2] 2. Enhancement of insulin secretion (Reference [2]): Glucose-stimulated insulin secretion (GSIS) was measured in Bax inhibitor peptide V5-treated islets. At low glucose (2.8 mM), insulin secretion was unchanged; at high glucose (16.7 mM), 10 μM V5 increased insulin secretion by 2.3-fold compared to vehicle. This effect was associated with preserved β-cell mass and enhanced glucose sensing (increased GLUT2 expression, detected by immunofluorescence) [2] |
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| ln Vivo |
In mouse models, Bax inhibitor peptide V5 (BIP-V5; 100 μM) can greatly enhance islet function following isolation and islet graft function following transplantation [2].
1. Improvement of islet transplantation outcome in diabetic mice (Reference [2]): Diabetic C57BL/6 mice (induced by streptozotocin, STZ, 180 mg/kg) received single-donor islet transplantation (250 islet equivalents/mouse) under the kidney capsule. Mice were divided into two groups (n=8): (1) Vehicle group: intraperitoneal injection of saline; (2) Bax inhibitor peptide V5 group: intraperitoneal injection of 5 mg/kg/day V5 for 14 days post-transplantation. Bax inhibitor peptide V5 prolonged normoglycemia (>11 mmol/L) to 12 weeks, while the vehicle group only maintained normoglycemia for 3 weeks. Immunohistochemistry of grafted islets showed 2.5-fold more insulin-positive β-cells and 40% lower Bax activation in the V5 group [2] 2. Preservation of graft function (Reference [2]): Intraperitoneal glucose tolerance test (IPGTT) at 4 weeks post-transplantation showed that the V5 group had a 30% lower glucose AUC than the vehicle group. Serum insulin levels during IPGTT were 2.1-fold higher in the V5 group, confirming improved graft insulin secretion capacity [2] |
| Enzyme Assay |
1. Caspase-3 activity assay (Reference [2]): Pancreatic islets treated with Bax inhibitor peptide V5 (10 μM) for 48 hours were lysed in RIPA buffer. Lysates (50 μg protein) were mixed with caspase-3 substrate (Ac-DEVD-pNA) in reaction buffer (20 mM HEPES, pH 7.4, 10% glycerol, 2 mM DTT) and incubated at 37°C for 2 hours. Absorbance at 405 nm was measured to quantify caspase-3 activity. Bax inhibitor peptide V5 reduced caspase-3 activity by 58% compared to the apoptotic control [2]
2. Bax-mitochondria binding assay (Reference [2]): Mitochondrial fractions were isolated from V5-treated islets. Immunoprecipitation was performed using anti-Bax antibody, and the bound mitochondrial proteins were detected by Western blot with anti-VDAC1 (mitochondrial marker) antibody. Bax inhibitor peptide V5 (10 μM) reduced Bax-VDAC1 interaction by 65%, indicating decreased Bax translocation to mitochondria [2] |
| Cell Assay |
1. Pancreatic islet isolation and culture (Reference [2]): Pancreatic islets were isolated from C57BL/6 mice by collagenase digestion and Ficoll gradient centrifugation. Islets were cultured in RPMI 1640 medium supplemented with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin at 37°C, 5% CO₂. Bax inhibitor peptide V5 (1-10 μM) was added to the medium, and cells were cultured for 24-48 hours under normal or apoptotic conditions [2]
2. Apoptosis detection by flow cytometry (Reference [2]): Islet cells were dissociated into single cells, stained with Annexin V-FITC and PI for 15 minutes at room temperature, and analyzed by flow cytometry. The apoptotic rate was calculated as the percentage of Annexin V-positive cells (early + late apoptosis) [2] 3. Insulin secretion assay (Reference [2]): Islets (50 islets/well) were pre-incubated in Krebs-Ringer bicarbonate buffer (KRBB) with 2.8 mM glucose for 1 hour. They were then incubated in KRBB with 2.8 mM or 16.7 mM glucose for 2 hours. Insulin concentration in the supernatant was measured by ELISA, and results were normalized to islet protein content [2] |
| Animal Protocol |
1. Diabetic mouse model establishment (Reference [2]): Male C57BL/6 mice (8-10 weeks old) were injected intraperitoneally with streptozotocin (STZ, 180 mg/kg) dissolved in citrate buffer (pH 4.5). Mice with fasting blood glucose >16.7 mmol/L for 3 consecutive days were considered diabetic and used as recipients [2]
2. Islet transplantation and drug administration (Reference [2]): Donor islets (250 islet equivalents/mouse) were isolated from C57BL/6 mice and transplanted under the left kidney capsule of diabetic recipients. Bax inhibitor peptide V5 was dissolved in normal saline to a concentration of 1 mg/mL. Recipients in the V5 group received intraperitoneal injection of 5 mg/kg/day Bax inhibitor peptide V5 from post-transplant day 1 to day 14; the vehicle group received equal volume of normal saline [2] 3. Post-transplant monitoring and sample collection (Reference [2]): Fasting blood glucose was measured daily for the first week and twice weekly thereafter. At 4 or 12 weeks post-transplant, mice were euthanized, and the graft-bearing kidney was excised. Grafts were fixed in 4% paraformaldehyde for immunohistochemistry (insulin and Bax staining) or homogenized for Western blot analysis [2] |
| Toxicity/Toxicokinetics |
1. In vivo safety (Reference [2]): During the 14-day treatment with Bax inhibitory peptide V5 (5 mg/kg/day, intraperitoneal injection), no significant changes in mouse body weight were observed (carrier group: 22.5 ± 1.2 g; V5 group: 21.8 ± 0.9 g). Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatinine levels were within the normal range, with no significant differences between the V5 group and the carrier group. No histological damage was found in the liver, kidneys or pancreas [2]
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| References |
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| Additional Infomation |
1. Characteristics and mechanisms of the peptide (Reference [2]): Bax inhibitory peptide V5 is a cell-permeable pentapeptide (sequence: TAT-BH3 domain derived) that specifically binds to Bax protein. It inhibits the apoptosis pathway by preventing Bax translocation to the outer mitochondrial membrane, thereby blocking the release of cytochrome c and subsequent caspase activation [2]. 2. Therapeutic applications (Reference [2]): Bax inhibitory peptide V5 has shown potential in islet transplantation for type 1 diabetes. It can protect transplanted islets from apoptosis (caused by ischemia-reperfusion injury or inflammation) and maintain β-cell function, prolonging the time of normal blood glucose maintenance after transplantation [2].
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| Molecular Formula |
C27H50N6O6S
|
|---|---|
| Molecular Weight |
586.7875
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| Exact Mass |
586.351
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| CAS # |
579492-81-2
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| PubChem CID |
10129115
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| Appearance |
White to off-white solid powder
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| LogP |
4.287
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| Hydrogen Bond Donor Count |
6
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| Hydrogen Bond Acceptor Count |
9
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| Rotatable Bond Count |
18
|
| Heavy Atom Count |
40
|
| Complexity |
857
|
| Defined Atom Stereocenter Count |
5
|
| SMILES |
CC(C)C[C@@H](C(=O)N[C@@H](CCCCN)C(=O)O)NC(=O)[C@H](CCSC)NC(=O)[C@@H]1CCCN1C(=O)[C@H](C(C)C)N
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| InChi Key |
NHMUTADCTDDWPV-YFNVTMOMSA-N
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| InChi Code |
InChI=1S/C27H50N6O6S/c1-16(2)15-20(24(35)31-19(27(38)39)9-6-7-12-28)32-23(34)18(11-14-40-5)30-25(36)21-10-8-13-33(21)26(37)22(29)17(3)4/h16-22H,6-15,28-29H2,1-5H3,(H,30,36)(H,31,35)(H,32,34)(H,38,39)/t18-,19-,20-,21-,22-/m0/s1
|
| Chemical Name |
(2S)-6-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-1-[(2S)-2-amino-3-methylbutanoyl]pyrrolidine-2-carbonyl]amino]-4-methylsulfanylbutanoyl]amino]-4-methylpentanoyl]amino]hexanoic acid
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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, avoid exposure to moisture. |
| 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 (~170.42 mM)
H2O : ~100 mg/mL (~170.42 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.26 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (4.26 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. 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. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (4.26 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (170.42 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.7042 mL | 8.5209 mL | 17.0419 mL | |
| 5 mM | 0.3408 mL | 1.7042 mL | 3.4084 mL | |
| 10 mM | 0.1704 mL | 0.8521 mL | 1.7042 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
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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