Cell apoptosis, sometimes called programmed cell death, is a cellular self-destruction method to remove old and damaged cells during development and aging to protect cells from external disturbances and maintain homeostasis. Apoptosis also occurs as a defense mechanism such as in immune reactions or when cells are damaged by disease or noxious agents.

Apoptosis is controlled by many genes and involves two fundamental pathways: the extrinsic pathway, which transmits death signals by the death receptor (DR), and the intrinsic or mitochondrial pathway. The extrinsic apoptotic pathway is activated by the binding of the death ligand to DRs, including FasL, TNF-α, and TRAIL, on the plasma membrane. The DR, adaptor protein (FADD), and associated apoptosis signaling molecule (caspase-8) form the death-inducing signaling complex (DISC), thus leading to the activation of the effector caspase cascade (caspase-3, -6, and -7). The mitochondria-mediated intrinsic apoptosis pathway is regulated by Bcl-2 family proteins, including proapoptotic (Bid, Bax, Bak) and antiapoptotic proteins (Bcl-2, Bcl-xL).

Abnormalities in cell apoptosis can be a significant component of diseases such as cancer, autoimmune lymphoproliferative syndrome, AIDS, ischemia, and neurode-generative diseases. These diseases may benefit from artificially inhibiting or activating apoptosis. A short list of potential methods of anti-apoptotic therapy includes stimulation of the IAP (inhibitors of apoptosis proteins) family of proteins, caspase inhibition, PARP (poly [ADP-ribose] polymerase) inhibition, stimulation of the PKB/Akt (protein kinase B) pathway, and inhibition of Bcl-2 proteins.

Ferroptosis and necroptosis are recently recognized forms of regulated cell death that differs considerably from apoptosis. Misregulated ferroptosis or necroptosis have also been implicated in multiple physiological and pathological processes, including cancer cell death, neurotoxicity, neurodegenerative diseases, etc.

References:
[1] Susan Elmore. Toxicol Pathol. 2007; 35(4): 495–516.
[2] Cao L, et al. J Cell Death. 2016 Dec 29;9:19-29.
[3] Dasgupta A, et al. Int J Mol Sci. 2017 Jan; 18(1): 23.
[4] Xie Y, et al. Cell Death Differ. 2016 Mar;23(3):369-79.


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FUBP1-IN-2

FUBP1-IN-2 (compound 9) is a potent FUBP1 (far upstream binding protein 1) inhibitor. FUBP1-IN-2 inhibits the KH4 FUBP1-FUSE interaction in a gel shift assay. FUBP1-IN-2 binds to FUBP1 in a ChIP assay. FUBP1-IN-2 reduces both c-Myc mRNA and protein expression, increases p21 mRNA and protein expression, and depletes intracellular polyamines[1].

  • CAS Number: 1242862-71-0
  • MF: C26H26ClN3O4
  • MW: 479.96
  • Catalog: c-Myc
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

KY-05009

KY-05009 is an ATP-competitive Traf2- and Nck-interacting kinase (TNIK) inhibitor with a Ki of 100 nM. KY-05009 pharmacologically inhibits TGF-β1-induced epithelial-to-mesenchymal transition (EMT) in human lung adenocarcinoma cells. KY-05009 inhibits the protein expression of TNIK and transcriptional activity of Wnt target genes and induces apoptosis in cancer cells. KY-05009 exerts anti-cancer activity[1].

  • CAS Number: 1228280-29-2
  • MF: C18H16N4O2S
  • MW: 352.410
  • Catalog: Apoptosis
  • Density: 1.4±0.1 g/cm3
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Casein Kinase inhibitor A51

Casein Kinase inhibitor A51 (CKIα inhibitor A51) is a novel pan-specific CKI (CSNK1) inhibitor (Kd=0.5-20 nM, CKIα Kd=5.3 nM) that co-targets the transcriptional kinases CDK7 and CDK9, with hardly inhibition of CDK8, CDK13, CDK11a, CDK11b, and CDK19; target both CDK7 and CDK9 with low nM Kd values; induces leukemia cell apoptosis at <160 nM, in correlation to the capacity to stabilize p53; shows high and selective sensitivity against leukemic CFUs in colony-forming unit (CFU) assay, without effect on normal hematopoietic CFUs; blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, induce apoptosis, abolishes the expression of MYC, MDM2, and the anti-apoptotic oncogene MCL1; demonstrates therapeutic efficacy with preserved hematopoiesis and leukemia cure potential in AML mouse models.

  • CAS Number: 2079068-74-7
  • MF: C18H25ClN6
  • MW: 360.89
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Amifostine thiol

Amifostine thiol (WR-1065) is an active metabolite of the cytoprotector Amifostine (HY-B0639). Amifostine thiol is a cytoprotective agent with radioprotective abilities. Amifostine thiol activates p53 through a JNK-dependent signaling pathway[1][2][3].

  • CAS Number: 31098-42-7
  • MF: C5H14N2S
  • MW: 134.24300
  • Catalog: MDM-2/p53
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

HC Toxin

HC-Toxin, a cyclic tetrapeptide, is a potent HDAC inhibitor with an IC50 of 30 nM[1]. HC-Toxin induces tumor cell apoptosis and has anticancer effects[2].

  • CAS Number: 83209-65-8
  • MF: C21H32N4O6
  • MW: 436.50
  • Catalog: Apoptosis
  • Density: 1.3±0.1 g/cm3
  • Boiling Point: 819.2±65.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 449.2±34.3 °C

5-NIdR

5-NIdR (1-(β-D-2-Deoxyribofuranosyl)-5-nitroindole), an artificial nucleoside, exhibits the ability to inhibit the replication of DNA lesions generated by Temozolomide (HY-17364). 5-NIdR induces cancer cells apoptosis and arrests cell cycle at G0 phase. 5-NIdR enhances Temozolomide anti-tumor efficacy in murine glioblastoma model[1].

  • CAS Number: 191421-10-0
  • MF: C13H14N2O5
  • MW: 278.26100
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Bisdemethoxycurcumin

Bisdemethoxycurcumin(Curcumin III; Didemethoxycurcumin) is a natural derivative of curcumin with anti-inflammatory and anti-cancer activities.IC50 value:Target: Anticancer natural compoundin vitro: BDMC-induced apoptosis was mediated by a combinatory inhibition of cytoprotective proteins, such as Bcl2 and heme oxygenase-1 and increased generation of reactive oxygen species. Intriguingly, BDMC-induced apoptosis was reversed with co-treatment of sr144528, a cannabinoid receptor (CBR) 2 antagonist, which was confirmed with genetic downregulation of the receptor using siCBR2 [1]. Induction of cell cycle arrest in HepG2 cells by NB and BDCur in combination was evidenced by accumulation of the G2/M cell population. Further investigation on the molecular mechanism showed that NB and BDCur in combination resulted in a significant decrease in the expression level of Cdc2 and cyclin B [2]. BDMC treatment activated Sirt1/AMPK signaling pathway. Moreover, downregulating Sirt1 by the pharmacological inhibitor nicotianamine or small interfering RNA blocked BDMC-mediated protection against t-BHP-mediated decrease in proliferation [4].in vivo: human gastric adenocarcinoma xenograft model was generated in vivo using nude mice and BDMC was observed to suppress the growth and activity of tumors, in addition to improving the physical and mental capacity of the mice [3].

  • CAS Number: 33171-05-0
  • MF: C19H16O4
  • MW: 308.328
  • Catalog: Apoptosis
  • Density: 1.3±0.1 g/cm3
  • Boiling Point: 551.3±45.0 °C at 760 mmHg
  • Melting Point: 221-223ºC
  • Flash Point: 301.3±25.2 °C

FC-116

FC-11 is a Tubulin inhibitor that effectively inhibits tumor growth in mice. FC-11 can also induce endoplasmic reticulum (ER) stress to generate excess reactive oxygen species (ROS), leading to mitochondrial damage, thereby promoting apoptosis in colorectal cancer (CRC) cells by targeting microtubules. FC-11 can be used in cancer research[1].

  • CAS Number: 2417298-29-2
  • MF: C21H20FNO4
  • MW: 369.39
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

1-Dehydro-6-gingerdione

6-Dehydrogingerdione sensitizes human hepatoblastoma hep G2 cells to TRAIL-induced apoptosis via reactive oxygen species-mediated increase of DR5[1].

  • CAS Number: 76060-35-0
  • MF: C17H22O4
  • MW: 290.35400
  • Catalog: Apoptosis
  • Density: 1.1±0.1 g/cm3
  • Boiling Point: 448.9±40.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 159.3±20.8 °C

AP 1903

Rimiducid (AP1903) is a dimerizer agent that acts by cross-linking the FKBP domains, initiating Fas signaling and hence apoptosis.

  • CAS Number: 195514-63-7
  • MF: C78H98N4O20
  • MW: 1411.627
  • Catalog: TNF Receptor
  • Density: 1.2±0.1 g/cm3
  • Boiling Point: 1307.5±65.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 744.5±34.3 °C

VAS 3947

VAS 3947, a specific NADPH oxidase (NOX) inhibitor, exerts a potent antiplatelet effect. VAS3947 induces apoptosis independently of anti-NOX activity, via UPR activation, mainly due to aggregation and misfolding of proteins[1][2].

  • CAS Number: 869853-70-3
  • MF: C14H10N6OS
  • MW: 310.334
  • Catalog: Apoptosis
  • Density: 1.6±0.1 g/cm3
  • Boiling Point: 577.8±60.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 303.3±32.9 °C

L-Ascorbic acid-13C-1

L-Ascorbic acid-13C-1 is the 13C labeled L-Ascorbic acid. L-Ascorbic acid (L-Ascorbate), an electron donor, is an endogenous antioxidant agent. L-Ascorbic acid inhibits selectively Cav3.2 channels with an IC50 of 6.5 μM. L-Ascorbic acid is also a collagen

  • CAS Number: 178101-89-8
  • MF: C6H8O6
  • MW: 176.12412
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Antitumor agent-56

Antitumor agent-56 (Compound 33) is a triptolide derivative with antitumor, anti-inflammatory and NO release activities. Antitumor agent-56 significantly inhibits the growth of melanoma. Antitumor agent-56 is orally active[1].

  • CAS Number: 2411579-53-6
  • MF: C28H28N2O10S
  • MW: 584.59
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

4,8-Dimethoxy-1-vinyl-9H-β-carboline

Dehydrocrenatidine, a natural alkaloid, is a specific JAK inhibitor. Dehydrocrenatidine inhibits voltage-gated sodium channels and ameliorates mechanic allodia in a rat model of neuropathic pain[1][2].

  • CAS Number: 65236-62-6
  • MF: C15H14N2O2
  • MW: 254.284
  • Catalog: Apoptosis
  • Density: 1.3±0.1 g/cm3
  • Boiling Point: 491.8±40.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 174.9±17.6 °C

Z-Leu-Leu-Nle-aldehyde

Z-LLNle-CHO (Z-Leu-Leu-Nle-CHO) is a γ-secretase inhibitor I. Z-LLNle-CHO induces caspase and ROS-dependent apoptosis by blocking the Akt-mediated pro-survival pathway. Z-LLNle-CHO can be used in cancer research, such as breast cancer and leukaemia[1][2].

  • CAS Number: 133407-83-7
  • MF: C26H41N3O5
  • MW: 475.62100
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

MSN-50

MSN-50 is a Bax and Bak oligomerization inhibitor. MSN-50 efficiently inhibits liposome permeabilization, prevents genotoxic cell death and promotes neuroprotection[1][2].

  • CAS Number: 1592908-75-2
  • MF: C36H38BrN3O6
  • MW: 688.61
  • Catalog: Bcl-2 Family
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Lacidipine-13C8

Lacidipine-13C8 is the deuterium labeled Lacidipine[1]. Lacidipine is an orally active and highly selective L-type calcium channel blocker that acts on smooth muscle calcium channels, primarily dilates peripheral arteries, reduces peripheral resistance, and has long-lasting anti-hypertensive activity. Lacidipine protects HKCs from apoptosis induced by ATP depletion and recovery by modulating the caspase-3 pathway. Lacidipine can be used in studies of hypertension, atherosclerosis and acute kidney injury (AKI)[2][3].

  • CAS Number: 1261432-01-2
  • MF: C1813C8H33NO6
  • MW: 463.48
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

PhiKan 083

PhiKan 083 hydrochloride is a carbazole derivative, which can stabilize Y220C (a p53 mutant), with a Kd of 167 μM measured by NMR, used for cancer research.

  • CAS Number: 1050480-30-2
  • MF: C16H19ClN2
  • MW: 274.789
  • Catalog: MDM-2/p53
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Daunorubicin citrate

Daunorubicin (Daunomycin) citrate is a topoisomerase II inhibitor with potent anti-tumor activity. Daunorubicin citrate inhibits DNA and RNA synthesis. Daunorubicin citrate is a cytotoxin that inhibits cancer cell viability and induces apoptosis and necrosis. Daunorubicin citrate is also an anthracycline antibiotic. Daunorubicin citrate can be used in the research of infection and variety of cancers, including leukemia, non-Hodgkin lymphomas, Ewing's sarcoma, Wilms' tumor[1][2][4][5].

  • CAS Number: 1884557-85-0
  • MF: C33H37NO17
  • MW: 719.64
  • Catalog: Bacterial
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

M 50054

M50054 is a potent inhibitor of apoptosis. M50054 inhibits Etoposide-induced caspase-3 activation of U937 cells with an IC50 of 79 μg/mL. M50054 does not directly inhibit the enzymatic activity of caspase-3. M50054 can be used for the research anti-Fas-antibody-induced hepatitis and chemotherapy-induced alopecia[1].

  • CAS Number: 54135-60-3
  • MF: C13H16O4
  • MW: 236.26400
  • Catalog: Apoptosis
  • Density: 1.227 g/cm3
  • Boiling Point: 461.2ºC at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 199ºC

Desmethylxanthohumol

Desmethylxanthohumol is a prenylated hydroxychalcone isolated from hop cones (Humulus lupulus L.). Desmethylxanthohumol is a powerful apoptosis inducing agent. Desmethylxanthohumol has antiplasmodial, antiproliferative, and antioxidant bioactivities[1][2].

  • CAS Number: 115063-39-3
  • MF: C20H20O5
  • MW: 340.37000
  • Catalog: Apoptosis
  • Density: 1.312g/cm3
  • Boiling Point: 570.7ºC at 760mmHg
  • Melting Point: N/A
  • Flash Point: 313ºC

MYCMI-6(NSC 354961)

MYCMI-6 (NSC354961) is a selective, high affinity inhibitor of MYC-MAX interaction, blocks MYC-driven transcription and binds selectively to the MYC bHLHZip domain with Kd of 1.6 uM in SPR assay; specifcally targets MYC:MAX interaction without interfering with other MYC activities, selectively suppresses MYC-driven tumor cell growth with high efficacy, efficiently inhibits anchorage-independent growth of MYCN-amplifed neuroblastoma cells with GI50 values of <0.4, 5 and 0.75 μM, respectively; reduces proliferation and induces massive apoptosis in tumor tissue from a MYC-driven xenograft tumor model without severe side effects

  • CAS Number: 681282-09-7
  • MF: C20H19N7O
  • MW: 373.42
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Glycochenodeoxycholic acid

Glycochenodeoxycholic acid is a bile salt formed in the liver from chenodeoxycholate and glycine; used to induce hepatocyte apoptosis in research.

  • CAS Number: 640-79-9
  • MF: C26H43NO5
  • MW: 449.62300
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Larotaxel

Larotaxel (XRP9881) is a taxane analogue with preclinical activity against taxane-resistant breast cancer. Larotaxel (XRP9881) exerts its cytotoxic effect by promoting tubulin assembly and stabilizing microtubules, ultimately leading to cell death by apoptosis. It presents the ability to cross the blood brain barrier and has a much lower affinity for P-glycoprotein 1 than Docetaxel[1][2][3].

  • CAS Number: 156294-36-9
  • MF: C45H53NO14
  • MW: 831.901
  • Catalog: Apoptosis
  • Density: 1.4±0.1 g/cm3
  • Boiling Point: 889.3±65.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 491.7±34.3 °C

HTH-01-091

HTH-01-091 is a potent and selective, cell-permeable, ATP-competitive MELK inhibitor with biochemical IC50 of 10.5 nM; displays no significant activity for PIK3CA, mTOR, GSK3A and CDK7 (IC50>600 nM); exhibits substantially improved kinome selectivity in comparison with OTSSP167; induces MELK degradation, but demonstrates poor antiproliferative effects in basal-like breast cancer cell lines.

  • CAS Number: 2000209-42-5
  • MF: C26H28Cl2N4O2
  • MW: 499.436
  • Catalog: RIP kinase
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Falcarindiol

Falcarindiol, an orally active polyacetylenic oxylipin, activates PPARγ and increases the expression of the cholesterol transporter ABCA1 in cells. Falcarindiol induces apoptosis and autophagy. Falcarindiol has anti-inflammatory, antifungal, anticancer and antidiabetic properties[1][2].

  • CAS Number: 55297-87-5
  • MF: C17H24O2
  • MW: 260.371
  • Catalog: Apoptosis
  • Density: 1.0±0.1 g/cm3
  • Boiling Point: 408.2±45.0 °C at 760 mmHg
  • Melting Point: N/A
  • Flash Point: 184.7±23.3 °C

Brentuximab

Brentuximab vedotin (cAC10-vcMMAE) is an antibody-drug conjugate (ADC) comprising an anti-CD30 antibody and the cytotoxic agent Monomethyl auristatin E (MMAE). Brentuximab vedotin inhibits CD30-positive cells with an IC50 of 2.5 ng/mL. Brentuximab vedotin can be used for the research of relapsed and refractory Hodgkin lymphoma[1][2].

  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

(R)-Humulone

Humulone (α-Lupulic acid), a prenylated phloroglucinol derivative, is a potent cyclooxygenase-2 (COX-2) inhibitor. Humulone acts as a positive modulator of GABAA receptor at low micromolar concentrations. Humulone is an inhibitor of bone resorption. Humulone possesses antioxidant, anti-angiogenic and apoptosis-inducing properties[1][2][3].

  • CAS Number: 26472-41-3
  • MF: C21H30O5
  • MW: 362.460
  • Catalog: Apoptosis
  • Density: 1.2±0.1 g/cm3
  • Boiling Point: 571.4±50.0 °C at 760 mmHg
  • Melting Point: 65-66.5℃
  • Flash Point: 313.4±26.6 °C

Tubulysin I

Tubulysin I is a highly cytotoxic peptide isolated from the myxobacterial species Archangium geophyra and Angiococcus disciformis. Tubulysin displays extremely potent cytotoxic activity in mammalian cells, including multidrug-resistant cell lines, with IC50 values in the lower nanomolar range[1]. Tubulysin I is a cytotoxic activity tubulysin which inhibits tubulin polymerization and leads to cell cycle arrest and apoptosis[2].

  • CAS Number: 799822-10-9
  • MF: C40H59N5O10S
  • MW: 801.99
  • Catalog: Apoptosis
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A

Oenothein B

Oenothein B is a dimeric macrocyclic ellagitannin and has widely pharmacological activities, including antioxidant, anti-inflammatory, antifungal, anti-HCV, and antitumor properties. Oenothein B is a potent and specific inhibitor of poly(ADP-ribose) glycohydrolase[1][2].

  • CAS Number: 104987-36-2
  • MF: C68H48O44
  • MW: 1569.08000
  • Catalog: Bacterial
  • Density: N/A
  • Boiling Point: N/A
  • Melting Point: N/A
  • Flash Point: N/A