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Apoptosis Inducers

Activation and Inhibition of Apoptosis
Several mechanisms have been identified in mammalian cells for the induction of apoptosis. These mechanisms include factors that lead to perturbation of the mitochondria leading to leakage of cytochrome c or factors that directly activate members of the death receptor family. Fas is a member of the tumor necrosis factor (TNF) receptor superfamily, a family of transmembrane receptors that include neurotrophin receptor (p75NTR), TNF-R1, and a variety of other cell surface receptors. Fas Ligand (Fas L) transmits signals to Fas on a target cell by inducing trimerization of Fas. Activation of Fas causes the recruitment of Fas-associated protein with death domain (FADD) via interactions between the death domain of Fas and FADD and is followed by pro-caspase-8 binding to FADD via interactions between the death effector domains (DED) of FADD and pro-caspase-8 leading to the activation of caspase-8. Activation of caspase-8 leads to the activation of other caspases, in effect beginning a caspase cascade that ultimately leads to apoptosis. Caspase-8 activation can also activate Bid, leading to activation of the apoptotic program. Fas-induced apoptosis can be effectively blocked at several stages by either FLICE-inhibitory protein (FLIP), by Bcl-2, or by the cytokine response modifier A (CrmA). In addition, activation of caspase-3 by caspase-9 can be blocked by inhibitor of apoptosis proteins (IAPs). Moreover, the protein kinase, Akt, can be activated by various growth factors and its activity can be blocked by PTEN. Akt functions to promote cell survival through two distinct pathways. Akt inhibits apoptosis by phosphorylating the Bcl-2 family member Bad, which then interacts with 14-3-3 and dissociates from Bcl-xL allowing for cell survival. Alternatively, Akt activates IKK-α that ultimately leads to NF-κB activation and cell survival. Proapoptotic Bcl-2 family members, such as Bax and Bak can promote mitochondrial permeability, while Bcl-2 can inhibit their effects. Upon mitochondrial permeability, apoptogenic factors are released from the mitochondrial inter-membrane space and leak into the cytosol. One factor is cytochrome c, which induces the liberation of protease activators (caspases) that ultimately lead to apoptosis through nuclear damage (DNA fragmentation, DNA mutations). In addition, Smac/Diablo is released and can block IAP inhibition of caspase activity. Mitochondrial permeability is also related to the increased generation of reactive oxygen species (ROS), which plays a role in the degradation phase of apoptosis (i.e. plasma membrane alterations).


Caspase Independent Apoptosis

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Description
Biochem/physiol Actions
solubility
Product #
17-(Allylamino)-17-demethoxygeldanamycin ≥98% (HPLC), solid Potent inhibitor of heat shock protein 90 (Hsp90). 17-AAG is a less toxic analog than geldanamycin. It induces apoptosis and displays antitumor effects. 17-AAG inhibits the activity of oncogenic proteins such as N-ras, Ki-ras, c-Akt, and p185erB2.
 DMSO: soluble
methanol: soluble
 A8476
2-Amino-N-quinolin-8-yl-benzenesulfonamide ≥98% (HPLC), solid Inhibitor of cell cycle at G2 phase; apoptosis inducer.
 DMSO: 22 mg/mL, soluble
H2O: insoluble
 A3105
BH3I-1 ≥97% (HPLC), powder, yellow Synthetic cell permeable Bcl-xL antagonist; apoptosis inducer.
 DMSO: >10 mg/mL, soluble
H2O: insoluble
 B8809
Borrelidin from Streptomyces parvulus, ≥98% (HPLC) Borrelidin, an 18-membered macrolide-polyketide, is a compound with anti-viral, anti-bacterial, anti-malarial, and anti-angiogenic properties. It is a known inhibitor of bacterial and eukaryal threonyl-tRNA synthetases. Borrelidin induces apoptosis in endothelial cells via the caspase 3 and caspase 8 pathway. In addition, borrelidin strongly inhibits capillary tube formation and also disrupts formed capillary tubes by inducing apoptosis of the tube-forming cells in a rat aorta matrix culture model. In S.cerevisiae, borrelidin inhibits the cyclin-dependent kinase Cdc28/Cln2 with an IC50 of 24 μM, causing the arrest of both haploid and diploid cells in G1 phase and inducing the transcription of amino acid biosynthetic enzymes through a GCN4-dependent pathway.
 DMSO: 1 mg/mL
methanol: 1 mg/mL
 B3061
Borrelidin from Streptomyces sp., ≥95% (HPLC), lyophilized powder Borrelidin, an 18-membered macrolide-polyketide, is a compound with anti-viral, anti-bacterial, anti-malarial, and anti-angiogenic properties. It is a known inhibitor of bacterial and eukaryal threonyl-tRNA synthetases. Borrelidin induces apoptosis in endothelial cells via the caspase 3 and caspase 8 pathway. In addition, borrelidin strongly inhibits capillary tube formation and also disrupts formed capillary tubes by inducing apoptosis of the tube-forming cells in a rat aorta matrix culture model. In S.cerevisiae, borrelidin inhibits the cyclin-dependent kinase Cdc28/Cln2 with an IC50 of 24 μM, causing the arrest of both haploid and diploid cells in G1 phase and inducing the transcription of amino acid biosynthetic enzymes through a GCN4-dependent pathway.
 DMF: soluble
DMSO: soluble
ethanol: soluble
ethyl acetate: soluble
methanol: soluble
 B1936
Brefeldin A from Penicillium brefeldianum, Ready Made Solution, 10 mg/mL in DMSO, 0.2 μm filtered Brefeldin A (BFA) is a fungal metabolite which disrupts the structure and function of the Golgi apparatus. BFA is an activator of the sphingomyelin cycle. Brefeldin A-mediated apoptosis has been observed in human tumor cells.
 B5936
Bufalin B0261
CD437 ≥98% (HPLC), solid CD437 hemihydrate is a retinoic acid receptor, γ-selective retinoid; potent inducer of apoptosis in human lung, cervical, and breast cancer cells.
 DMSO: >10 mg/mL
H2O: insoluble
 C5865
CHM-1 hydrate ≥99% (HPLC), solid New CHM-1 possess antimitotic antitumor activity. It is a potent and selective antitumor agent in human hepatocellular carcinoma. CHM-1 induces apoptosis, and it binds tubulin and inhibits tubulin polymerization.
 DMSO: ≥5 mg/mL
 C1244
CIL-102 ≥95% (HPLC), solid Tubulin polymerization inhibitor: apoptosis inducer.
 DMSO: 12 mg/mL
 C5492
Carboxyatractyloside potassium salt ≥98% (HPLC), from Xanthium sibiricum, solid Carboxylatractyloside is a highly selective inhibitor of cytosolic side-specific mitochondrial ADP/ATP carrier; i.e. adenine nucleotide translocase (ANT); causes stabilization of the c conformation of ANT leading to permeability transition pore (PTP) opening, loss of mitochondrial membrane potential, and apoptosis.
 H2O: >10 mg/mL
 C4992
DMXAA ≥98% (HPLC), solid Apoptosis inducer; anti-vascular.
 DMSO: >10 mg/mL, soluble
 D5817
Erastin ≥98% (HPLC), powder Erastin is an antitumor agent selective for tumor cells bearing oncogenic RAS (i.e. HRAS, KRAS). Erastin produces non-apoptotic tumor cell death by altering mitochondrial voltage-dependent anion channel (VDAC) gating allowing cations to enter mitochondria and leading to release of oxidative species causing oxidative cell death.
 DMSO: >10 mg/mL
 E7781
Fluticasone propionate ≥98% (HPLC), solid Second generation glucocorticoid. Used as an anti-inflammatory agent for asthma. Shown to enhance eosinophil apoptosis in a concentration-dependent manner via the glucocorticoid receptor.
 DMSO: ≥10 mg/mL
 F9428
HA 14-1 ≥94% (HPLC), powder HA 14-1 is a nonpeptide apoptosis inducer; Bcl-2 antagonist.
 DMSO: 26 mg/mL
 H8787
HMBA ≥98% (HPLC), solid Inhibitor of microtubule polymerization1; apoptosis inducer.
 DMSO: 34 mg/mL, soluble
 H4663
Imiquimod ≥98% (HPLC), solid Imiquimod is a caspase 3 activator, which directly induces procaspase 3 cleavage to active caspase 3. Imiquimod induces apoptosis in vivo in basal cell carcinoma. Its anti-tumor activity is related to the induction of apoptosis. Imiquimod has anti-angiogenic, anti-inflammatory, anti-viral activities. Imiquimod also acts as an immune response modulator inducing the secretion of various cytokines and chemokines.
 DMSO: 4 mg/mL warming to 60 °C for 15 minutes
H2O: <2 mg/mL
 I5159
Muristerone A ≥90% Native phytosteroid known to have insecticidal properties. Induces apoptosis in cell transfected with wild-type Bax and ecdysone-inducible gene expression systems in mammalian cells and transgenic animals.
 M7888
Neocarzinostatin from Streptomyces carzinostaticus ≥90% (SDS-PAGE), ~0.5 mg/mL Neocarzinostatin is a protein-small molecule complex composed of an enediyne chromophore tightly bound to a 113 amino acid single chain protein. The complex possesses antiproliferative and antitumor activity. The chromophore is the active compound, which is responsible for DNA cleavage; while the apoprotein stabilizes and regulates the availability of the labile chromophore. NCS chromophore is bound non-covalently in a cleft of the binding protein and is dissociable. Upon addition of a thiol, the chromophore forms a highly reactive biradical species that can induce sequence-specific single and double strand breaks in DNA. Neocarzinostatin inhibits DNA synthesis and possesses antitumor activity in various human and animal tumors. NCS inhibits cellular proliferation by inducing G2 cell cycle arrest and apoptosis in both human papillomavirus (HPV) positive and negative cell lines.
 N9162
Nutlin-3 ≥98% (HPLC), solid Nutlin-3 is a Mdm2 (mouse double minute 2) antagonist, p53 pathway activator, and apoptosis inducer.
 DMSO: 20 mg/mL
H2O: insoluble
 N6287
PETCM ≥98% (HPLC), solid Apoptosis inducer; caspase 3 activator. Antagonizes prothymocin-α (ProT-α, oncoprotein) inhibition of apoptosome formation.
 DMSO: 22 mg/mL, soluble
 P0871
PRIMA-1 ≥98% (HPLC), solid New PRIMA-1 is a selective re-activator of mutant p53 activity in tumor cells, and an inducer of apoptosis and inhibitor of growth of human tumors with mutant p53. Mutations in the tumor suppressor p53 take place in >50% tumor cells. PRIMA-1 selectively restores sequence-specific DNA binding and transactivational activity to mutant p53 proteins at µM concentrations. It works as a re-activator of the apoptotic function of mutant p53 via conformational modulation of function-specific epitopes.
 H2O: >10 mg/mL
 P0069
Prodigiosin hydrochloride from Serratia marcescens, ≥98% (HPLC), liquid New Prodigiosin, a tripyrrole red pigment biosynthesized by Serratia marcescens and other bacteria, exhibits antibacterial, anticancer, cytotoxic, immunosuppressive, and antiproliferative activities.1,2,3 Prodigiosin induces apoptosis in hematopoietic cancer cells and cells derived from other human cancers, including gastric and colon with no marked toxicity in nonmalignant cell lines.2,4,5 Morphological analysis of prodigiosin-treated cells demonstrated that prodigiosin induces cell shrinkage, chromatin condensation, reorganization of actin microfilament architecture, and detachment of cells from the cell culture substrate.6 Different targets and mechanisms of action are described for prodigiosin, including induction of single- and double-strand DNA breaks, modulation of pH, regulation of mitogen-activated protein kinase, and inhibition of cell cycle progression.5
 acetonitrile: soluble
chloroform: soluble
DMSO: soluble
H2O: insoluble
methanol: soluble
 P0103
Pterostilbene ≥97% (HPLC), solid Antioxidant, antiproliferative, apoptosis inducer, antihyperglycemic, antidiabetic.
 DMSO: >20 mg/mL
H2O: insoluble
 P1499
Ridaifen-B ≥98% (HPLC), white solid New Ridaifen-B (RID-B) is a novel tamoxifen (TAM) analog that significantly augments apoptosis-inducing effect of TAM in estrogen receptor (ER)-negatives cells. Ridaifen-B induces mitochondria-involved apoptosis in Jurkat cells, as evidenced by chromatin-condensed cells as well as downstream activation of caspases (caspase-3, -8 and -9) in a dose- and time-dependent manner. At 4 hours of incubation, IC50 for RID-B is 4 muM (30 muM for TAM). And at prolonged treatment of 48 hours, IC50 for RID-B is 0.1 muM.1 In a related report2 on the global anti-tumor activity, RID-B strongly inhibits 39 human cancer cells (JFCR 39), both ER-+ or ER-- at concentrations of equal or less than 1muM (e.g., at 0.38muM for SF-539 [central nervous system], at 0.58muM for HT-29 [colon], at 0.20muM for DMS114 [lung], at 0.21muM for LOX-IMVI [melanoma], and at 0.23muM for MKN74 [stomach]. The binding protein of RID-B that exerts the apoptosis events is currently under investigation.
 DMSO: ≥13 mg/mL
H2O: insoluble
 R5030
Rifabutin >98% (HPLC), solid New Rifabutin is an antibiotic; antitumor. Rifabutin interferes with HSP-90 molecular chaperone, enhances ubiquitination and protein degradation, and inactivates bacterial RNA polymerase.
 DMSO: >5 mg/mL
 R3530
Temozolomide ≥98% (HPLC), solid Temozolomide is a DNA methylating agent and drug resistance-modifying agent; anti-tumor and anti-angiogenic. Temozolomide induces G2/M arrest and apoptosis through adduction of a methyl group to O6 position of guanine in genomic DNA and functional inactivation of DNA repair protein O(6)-alkylguanine DNA alkyltransferase (AGT) in base excision repair (BER) pathway.
 DMSO: >20 mg/mL
H2O: insoluble
 T2577

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