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Apoptosis Inhibitors

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Image	Description	Biochem/physiol Actions	solubility	Product #
	10058-F4 ≥98% (HPLC), solid	10058-F4 is a c-Myc inhibitor that induces cell-cycle arrest and apoptosis. It is a cell-permeable thiazolidinone that specificallly inhibits the c-Myc-Max interaction and prevents transactivation of c-Myc target gene expression. 10058-F4 inhibits tumor cell growth in a c-Myc-dependent manner both in vitro and in vivo (64 mM using c-Myc transfected Rat1a fibroblasts).	DMSO: >10 mg/mL H₂O: <2 mg/mL	F3680
	BAX Inhibiting Peptide V5 ≥97% (HPLC), lyophilized powder	Bax-mediated apoptosis inhibitor; membrane permeable pentapeptide based on the Ku70-Bax inhibiting domain.		B1436
	BBMP ≥98% (HPLC), solid	BBMP is a mitochondrial permeability transition pore (PTP) inhibitor. PTP inhibitors and mitochondrial depolarization are potential therapeutics for neurodegenerative diseases.	DMSO: 16 mg/mL H₂O: <2 mg/mL	B7936
	BI-6C9 ≥97% (HPLC), solid	BI-6C9 is a tBid inhibitor and antiapoptotic.	DMSO: 24 mg/mL H₂O: insoluble	B0186
	Bongkrekic acid solution from Pseudomonas cocovenenans, ≥95% (HPLC), ~1 mg/mL	An antiapoptotic agent, it protects against NMDA receptor induced neuronal apoptosis, extends cell survival in cells undergoing apoptosis following infection with viral vectors and abrogates apoptosis induced by hydrogen peroxide in T-cells. It is an inhibitor of adenine nucleotide translocase, which is a component of the mitochondrial permeability transition (MPT) pore complex. Bongkrekic acid prevents mitochondrial depolarization, swelling, rupture of mitochondrial outer membrane, and release of apoptogenic proteins such as cytochrome c. This phenomenon was observed during staurosporine induced apoptosis in Jurkat cells, in HepG2 undergoing apoptosis following TNF-α and ethanol.		B6179
	Cyclic Pifithrin-α >95% (HPLC)	A stable analog of Pifithrin-α (Product Code P4359) with similar biological activities and lower cellular toxicity.	DMSO: 20 mg/mL	P4236
	GNF-2 ≥98% (HPLC), solid	GNF-2 belongs to a new class of Bcr-abl inhibitors. GNF-2 appears to bind to the myristoyl binding pocket, an allosteric site distant from the active site, stabilizing the inactive form of the kinase. It inhibits Bcr-abl phosphorylation with an IC₅₀ of 267 nM, but does not inhibit a panel of 63 other kinases, including native c-Abl, and shows complete lack of toxicity towards cells not expressing Bcr-Abl. GNF-2 shows great potential for a new class of inhibitor to study Bcr-abl activity and to treat resistant Chronic myelogenous leukemia (CML), which is caused the Bcr-Abl oncoprotein.	DMSO: >5 mg/mL H₂O: <2 mg/mL	G9420
	MDL 28170 ≥95% (HPLC)	Potent cell permeable calpain I and II inhibitor; reduces capsaicin-mediated cell death in cultured dorsal root ganglion neurons. Reduced occurrence of apoptosis in H₂O₂ and A23187 treated PC12 cells. γ-secretase-inhibitor.	DMSO: 26 mg/mL H₂O: insoluble methanol: soluble	M6690
	N-Ethylmaleimide SigmaUltra, ≥98% (HPLC)	Augments currents from native M-channels in sympathetic neurons and acts as an opener for KCNQ2, KCNQ4 and KCNQ5 channels. Sulfhydryl alkylating agent that inactivates NADP-dependent isocitrate dehydrogenase and many endonucleases.	95% ethanol: 50 mg/mL colorless to faint yellow, clear to slightly hazy	E1271
	N-Ethylmaleimide crystalline, ≥98% (HPLC)	Augments currents from native M-channels in sympathetic neurons and acts as an opener for KCNQ2, KCNQ4 and KCNQ5 channels. Sulfhydryl alkylating agent that inactivates NADP-dependent isocitrate dehydrogenase and many endonucleases.		E3876
	NS3694 ≥98%, solid	Inhibitor of apoptosome formation.	DMSO: 22 mg/mL, soluble H₂O: <5 mg/mL, insoluble	N7787
	NSCI ≥97% (HPLC), solid	NSCI is a nonpeptide caspase 3 selective inhibitor.	DMSO: >10 mg/mL H₂O: insoluble	N1413
	Necrostatin-1 ≥98% (HPLC), solid	Necrostatin-1 is an inhibitor of necroptosis (non-apoptotic cell death pathway).	DMSO: >10 mg/mL	N9037
	Pifithrin-α ≥95% (HPLC), powder	Pifithrin-α is a reversible inhibitor of p53-mediated apoptosis and p53-dependent gene transcription such as cyclin G, p21/waf1, and mdm2 expression. Pifithrin-α enhances cell survival after genotoxic stress such as UV irradiation and treatment with cytotoxic compounds including doxorubicin, etopoxide, paclitaxel, and cytosine-β-D-arabinofuranoside. Pifithrin-α protects mice from lethal whole body γ-irradiation without an increase in cancer incidence. The protective effect is not seen in p53-null mice or cells expressing a dominant negative mutant of the p53 gene. Protection is conferred by the transient expression of p53 in p53-deficient cell lines.	DMSO: 20 mg/mL	P4359
	Pifithrin-μ ≥97% (HPLC), solid	Pifithrin-μ is an inhibitor of p53 binding and anti-apoptotic, which directly inhibits p53 binding to mitochondria as well as to Bcl-xL and Bcl-2 proteins. PFTμ rescues cells from lethal γ-irradiation-induced cell death. Because pifithrin-μ shuts down only the p53-mitochondrial pathway without affecting the transcriptional functions of p53, it is superior to pifithrin-α.	DMSO: >10 mg/mL H₂O: <2 mg/mL	P0122
	R5C3 ≥97% (HPLC), solid	MDM2 inhibitor, 2-phenoxybenzoyl-tryptophan derivative. Reported as a novel probe for high throughput fluorescence polarization binding assay. Useful in drug screening for small molecule inhibitors of MDM2-binding to p53.	DMSO: 18 mg/mL	R7529
	S-15176 difumarate salt ≥98% (HPLC), solid	Antioxidant and anti-ischemic agent. Also inhibits mitochondrial permeability transition, prevents the early step in apoptosis by preventing collapse of the electrochemical gradient across the mitochondrial membrane. IC₅₀ for in vitro lipid peroxidation is 0.3 μM. IC₅₀ for carnitine palmitoyltransferase (CPT-1) in heart homogenate is 16.8 μM. The shift from fatty acid to glucose oxidation may contribute to anti-ischemic effect.	DMSO: 16 mg/mL, soluble H₂O: insoluble	S5944

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