Bax inhibitor peptide P5Bax inhibitor CAS# 579492-83-4 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 579492-83-4 | SDF | Download SDF |
| PubChem ID | 10218792 | Appearance | Powder |
| Formula | C27H48N6O8S | M.Wt | 616.77 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | >61.7mg/mL in DMSO or water | ||
| Chemical Name | (2S)-2-[[(2S)-6-amino-2-[[(2S)-4-methyl-2-[[(2S)-4-methylsulfanyl-2-[[(2S)-pyrrolidine-2-carbonyl]amino]butanoyl]amino]pentanoyl]amino]hexanoyl]amino]pentanedioic acid | ||
| SMILES | CC(C)CC(C(=O)NC(CCCCN)C(=O)NC(CCC(=O)O)C(=O)O)NC(=O)C(CCSC)NC(=O)C1CCCN1 | ||
| Standard InChIKey | GAQGZEPUTWPXOG-SXYSDOLCSA-N | ||
| Standard InChI | InChI=1S/C27H48N6O8S/c1-16(2)15-21(33-25(38)19(11-14-42-3)31-23(36)17-8-6-13-29-17)26(39)30-18(7-4-5-12-28)24(37)32-20(27(40)41)9-10-22(34)35/h16-21,29H,4-15,28H2,1-3H3,(H,30,39)(H,31,36)(H,32,37)(H,33,38)(H,34,35)(H,40,41)/t17-,18-,19-,20-,21-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Originally reported to be a cell-permeable synthetic peptide inhibitor of Bax that blocks apoptosis. Also available: Bax inhibitor peptide V5 and Negative control . |
Bax inhibitor peptide P5 Dilution Calculator
Bax inhibitor peptide P5 Molarity Calculator
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Bax inhibitor peptide P5 (BIP P5) is a peptide inhibitor of Bax translocation to mitochondria [1].
Bax is a pro-apoptotic member of Bcl-2 family proteins and plays an important role in mitochondria-dependent apoptosis. Bax stays in the cytosol and transfers into mitochondria after apoptotic stimuli [1].
BIP P5 is a membrane-permeable peptide inhibitor of Bax translocation to mitochondria. In HeLa cells, BIP P5 protected cells from UVC- and STS-induced apoptosis. In U87-MG glioma cells, MCF-7 breast cancer cells and LNCaP prostate cancer cells, BIP P5 also inhibited apoptosis induced by anti-cancer drugs cisplatin, etoposide and doxorubicin. While BIP P5 did not suppress UVC- or STS-induced apoptosis in Bax-deficient cells (DU145), which suggested BIP P5 only suppressed Bax-mediated apoptosis. The caspase activation and the release of cytochrome c from mitochondria triggered by apoptotic stimuli were also significantly inhibited by BIP P5. BIP P5 inhibited the interaction of Ku70 and endogenous Bax in a dose-dependent way [1].
Reference:
[1]. Sawada M, Hayes P, Matsuyama S. Cytoprotective membrane-permeable peptides designed from the Bax-binding domain of Ku70. Nat Cell Biol, 2003, 5(4): 352-357.
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Mitochondrial regulation of insect cell apoptosis: evidence for permeability transition pore-independent cytochrome-c release in the Lepidopteran Sf9 cells.[Pubmed:19146980]
Int J Biochem Cell Biol. 2009 Jun;41(6):1430-40.
Role of cytochrome-c in insect cell apoptosis is highly controversial, with many earlier reports suggesting lack of involvement of mitochondrial factors in Drosophila while more recent studies have indicated otherwise, thus warranting more in-depth studies of insect cell apoptosis. In the present study, we investigated mitochondrial involvement during actinomycin-D induced apoptosis in Sf9 Lepidopteran cells. Cytochrome-c was released from mitochondria very early during apoptosis, and was preceded quickly by ROS generation and cardiolipin peroxidation. Albeit cytochrome-c release and apoptosis induction were inhibited by bongkrkicacid (BKA) it appears that the release is independent of permeability transition pore (PTP) as it preceded mitochondrial Ca(2+) buildup and mitochondrial membrane potential (MMP) loss. Further, the release was found to be unaffected by PTP inhibitor cyclosporin-A. Bax inhibitory peptide BiP-P5 could effectively block both cytochrome-c release and apoptosis induction indicating dependence on Bax-channel formation. Inhibition of apoptosis by FSBA, a nucleotide analog that inhibits apoptosome formation through Apaf1 binding, suggested activity of apoptosome similar to mammalian cells. Mitochondria isolated from treated cells activated caspases in the cytosolic fraction of untreated cells while mitochondrial lysates of treated or untreated cells had similar effect. Sequestering cytochrome-c in mitochondrial lysates inhibited DEVDase activity, and addition of purified cytochrome-c and dATP to Sf9 cytosolic fraction induced DEVDase activity, suggesting that cytochrome-c may be exclusively required for Lepidopteran apoptosis. This is the first detailed study demonstrating mitochondrial regulation of Lepidopteran insect cell apoptosis, and reiterates its homology with mammalian cell apoptosis while showing distinctive differences from earlier reports in Drosophila.
