There are many forms of cell death, most of which can be triggered by a variety of stimuli and physiological conditions. The often compared are apoptosis and necrosis. Apoptosis has become the focus of research area due to its complex nature and the different roles of maintaining healthy and self-sustaining biological entities. On the other hand, necrosis is a form of cell damage against acute external injury and trauma, leading to passive cell death and causing an inflammatory response. 
The BCl-2 family has been identified as its important role in apoptosis. The BH domain promotes interaction of family members with one another and may be indicative of pro-apoptotic or anti-apoptotic functions. Usually the BCL-2 family have been classified into one of three subfamilies; anti-apoptosis, BH3 only (pro-apoptotic) and pro-apoptotic proteins. The great promise for cancer therapy has been shown in recent research about BCL-2 targeting.
In the cell cycle, apoptosis acts as a fail-safe measure to prevent fidelity and proliferation quality. Although a certain degree of genetic variation is allowed and evolution is promoted, regenerative cells with extensive genetic errors and cell damage are subject to apoptosis. P53 is the Key role in the cell cycle system which initiate the apoptosis in certain cell types. P53 is a widely studied tumor suppressor. The p53 tumor suppressor gene is most frequently mutated in cancer cells (mutation occurs in more than 50% of human cancers) , which makes the restriction mechanism ineffective. Tumorigenesis is likely to commence when the p53-based preventive system loses its function completely.
Expression of stimuli, such as DNA damage, hypoxia and activation of certain oncoproteins (eg, Myc, Ras) are dependent on the apoptotic pathway of p53 . The transactivation function of p53 plays an important role in inducing apoptosis, the pro-apoptotic proteins, Bax and lgF-Bp3, are transcriptional targets of p53. As a well-known tumor suppressor, p53 is recognized for its ability to initiate apoptosis in the cell cycle and its ability to induce cell arrest and DNA repair in regenerative cells. In addition to p53, there are many other cell cycle regulators that can affect apoptosis (eg, pRb, p21).
Many studies have emphasized the importance of apoptosis in the self-defense mechanism or immune system. The immune system is responsible for rendering the host resistant to a variety of external pathogens. Apoptosis is an integral part of the immune system and helps maintain the homeostasis of the immune system. Secondly, the immune system relies on apoptosis to eliminate unwanted functional maturation of T cells and B cells . Finally, apoptosis confers cytotoxicity to certain cell types (ie, cytotoxic T lymphocytes and natural killer cells). A well-coordinated disruption protocol allows these cells to destroy target cells while the target cells remain intact. Cytotoxic T lymphocytes (CTLs) can induce target cell death in two ways, one of which involves perforin and granzymes.
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ABT-263 also called Navitoclax is a potent and orally bioavailable Bcl-2 family inhibitor (Ki's of <1 nmol/L for Bcl-2, Bcl-xL, and Bcl-w). it maintains a high affinity for Bcl-xL, Bcl-2, and Bcl-w, (Ki ≤1 nmol/L), but binds more weakly to Mcl-1 and A1.
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Bcl-2 Inhibitor contains a mixture of two tautomers. A potent, cell-permeable, Bcl-2 inhibitor competes with Bak BH3 peptide for binding to Bcl-2 and Bcl-XL in vitro (IC50 =10 uM and 7 uM, respectively). Learn More
A-1155463 is a highly potent and selective BCL-XL inhibitor, A-1155463 shows picomolar binding affinity to BCL-XL (Ki = <0.01 nM), and >1000-fold weaker binding to BCL-2 (Ki = 80 nM) and related proteins BCL-W (Ki = 19 nM) and MCL-1 (Ki > 440 nM) Learn More
Jaceosidin is a pharmacologically active flavone derived from Artemisia argyi, inhibits phorbol-ester-induced upregulation of COX-2 and MMP-9 by blocking phosphorylation of ERK-1 and -2 in cultured human mammary epithelial cells. Learn More
BTSA1 is a pharmacologically optimized BAX activator that binds with high affinity and specificity to the N-terminal activation site and induces conformational changes to BAX leading to BAX-mediated apoptosis. It effectively promotes apoptosis in leukemia cell lines and patient samples while sparing healthy cells.
A-385358 is an inhibitor of Bcl-XL that enhances the in vitro cytotoxic activity of numerous chemotherapeutic agents (paclitaxel, etoposide, cisplatin, and doxorubicin) in several tumor cell lines. Learn More
(+)-Apogossypol is a potent inhibitor of Bcl-2 family proteins; competing with the BH3 peptide-binding sites on Bcl-2, Bcl-XL, Mcl-1, Bcl-W, and Bcl-B, but not Bfl-1, with IC50s of 0.5 to 2 μM. Learn More
A-1210477 is a potent and selective MCL-1 inhibitor. A-1210477 induces the hallmarks of intrinsic apoptosis and demonstrates single agent killing of multiple myeloma and non-small cell lung cancer cell lines. Learn More
Gambogic acid is a natural product isolated from the Garcinia hanburyi tree. Gambogic Acid activates caspases with EC50 of 0.78-1.64 μM and competitively inhibits Bcl-XL, Bcl-2, Bcl-W, Bcl-B, Bfl-1 and Mcl-1 with IC50 of 1.47, 1.21, 2.02, 0.66, 1.06 and 0.79 μM, respectively. Learn More
Bax inhibitor peptide P5, cell-permeable synthetic peptide inhibitor of Bax translocation to mitochondria; designed from Ku70, a protein that is suggested to suppress the mitochondrial translocation of Bax. Inhibits Bax-mediated apoptosis in vitro. Learn More
Bax inhibitor peptide V5, cell-permeable synthetic peptide inhibitor of Bax translocation to mitochondria; designed from Ku70, a protein that is suggested to suppress the mitochondrial translocation of Bax. Inhibits Bax-mediated apoptosis in vitro. Learn More
Bax inhibitor peptide, negative control, negative control peptide for the Bax inhibitor peptides V5 and P5 , which inhibit Bax translocation to mitochondria and Bax-mediated apoptosis in vitro. Learn More
Hua Xu, .et al. Preclinical Study Using ABT263 to Increase Sensitivity to Suppress Prostate Cancer Progression Via Targeting BCL2/ROS/USP26 Axis Through Altering ARv7 Protein Degradation, Cancers (Basel), 2020, Apr; 12(4): 831 PMID: 32235588
El-Ashmawy NE, .et al. Modulatory Effect of Silymarin on Apoptosis in Testosterone -Induced Benign Prostatic Hyperplasia in Rats, Pathol Oncol Res, 2020, Jan 4 PMID: 31902118
Fujiki K, .et al. Blockade of ALK4/5 signaling suppresses cadmium- and erastin-induced cell death in renal proximal tubular epithelial cells via distinct signaling mechanisms, Cell Death Differ, 2019, Feb 25 PMID: 30804470
Maeda N, .et al. Glucocorticoids potentiate the inhibitory capacity of programmed cell death 1 by up-regulating its expression on T cells, J Biol Chem, 2019, Nov 13. pii: jbc.RA119.010379 PMID: 31723031
Yeh HT, .et al. Flavopereirine induces cell cycle arrest and apoptosis via the AKT/p38 MAPK/ERK1/2 signaling pathway in human breast cancer cells, Eur J Pharmacol, 2019, Sep 10;863:172658 PMID: 31518562
Schneider D, .et al. The E3 ubiquitin ligase RNF40 suppresses apoptosis in colorectal cancer cells, Clin Epigenetics, 2019, Jul 2;11(1):98 PMID: 31266541
Miyazawa S, .et al. Vitamin K2 induces non-apoptotic cell death along with autophagosome formation in breast cancer cell lines, Breast Cancer, 2019, Oct 17 PMID: 31625014
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LY573636 is a potent anti-tumor agent, which causes growth arrest and apoptosis of a variety of human solid tumors in vitro and in vivo. LY573636-induced apoptosis occurs by a mitochondrial-targeted mechanism. Learn More
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