BCL6 PROTAC 1 is a selective B-cell lymphoma 6 (BCL6) PROTAC. BCL6 PROTAC 1 inhibits BCL6 cell reporter with an IC50 value of 8.8 µM. BCL6 PROTAC 1 significantly degrades BCL6 in diffuse large B-cell lymphoma (DLBCL) cell lines. BCL6 PROTAC 1 can be used in tumor related research[1].
A-1293102 is a potent and selective BCL-XL inhibitor that kills BCL-XL-dependent tumor cells[1].
TRP-601 is a caspase inhibitor.
BCL6-IN-5 is a potent BCL6 inhibitor exacted from patent WO2018215801A1, example 1n, has a pIC50 of 5.82[1].
MIM-1 is an inhibitor of myeloid cell factor 1 (Mcl-1).
XZ739, a CRBN-dependent PROTAC BCL-XL degrader with a DC50 value of 2.5 nM in MOLT-4 cells after 16 h treatment. XZ739 also induces cell death through caspase-mediated apoptosis[1].
S65487 (VOB560) sulfate is a potent and selective Bcl-2 inhibitor. S65487 sulfate is also active on BCL-2 mutations, such as G101V and D103Y. S65487 sulfate has poor affinity with MCL-1, BFL-1 and BCL-XL. S65487 sulfate induces apoptosis and has anticaner activities[1][2].
Apoptotic agent-2 (compound 14b) induces apoptosis by down-regulation of Bcl-2 and up-regulation of Bax and caspase-3. Apoptotic agent-2 exhibits anti-proliferative activities and can be used for cancer research[1].
Glycocholic acid is a bile acid with anticancer activity, targeting against pump resistance-related and non-pump resistance-related pathways.
AZD-5991 is a potent and selective Mcl-1 inhibitor with an IC50 of 0.7 nM in FRET assay and a Kd of 0.17 nM in surface plasmon resonance (SPR) assay.
AZD-5991 S-enantiomer is the less active enantiomer of AZD-5991. AZD-5991 S-enantiomer is a Mcl-1 inhibitor with an IC50 of 6.3 μM in FRET assay and a Kd of 0.98 μM in surface plasmon resonance (SPR) assay.
ABBV-167 is a phosphate prodrug of the BCL-2 inhibitor venetoclax.
PNT100 is a 24-base, chemically unmodified DNA oligonucleotide sequence that is complementary to the regulatory region upstream of the BCL-2 gene. Exposure of tumor cells to PNT100 results in suppression of proliferation and cell death.
Maritoclax (Marinopyrrole A) is a novel and specific Mcl-1 inhibitor with an IC50 value of 10.1 μM, and shows >8 fold selectivity than BCL-xl (IC50 > 80 μM).
(S)-Gossypol is the isomer of a natural product Gossypol. (S)-Gossypol binds to the BH3-binding groove of Bcl-xL and Bcl-2 proteins with high affinity.
Paris saponin VII (Chonglou Saponin VII) is a steroidal saponin isolated from the roots and rhizomes of Trillium tschonoskii Maxim. Paris saponin VII-induced apoptosis in K562/ADR cells is associated with Akt/MAPK and the inhibition of P-gp. Paris saponin VII attenuates mitochondrial membrane potential, increases the expression of apoptosis-related proteins, such as Bax and cytochrome c, and decreases the protein expression levels of Bcl-2, caspase-9, caspase-3, PARP-1, and p-Akt. Paris saponin VII induces a robust autophagy in K562/ADR cells and provides a biochemical basis in the treatment of leukemia[1].
M24 is a Mcl-1 selective inhibitor. M24 exhibits good binding affinity against Mcl-1 with Ki value of 0.33 μM. M24 exhibits good anti-proliferative activity and induce apoptosis in HepG2 cells[1].
Bufarenogin induces intrinsic apoptosis via Bax and ANT cooperation[1].
Bcl-2/Bcl-xl inhibitor 1 (compound 6) is a dual Bcl-2 and Bcl-xl inhibitor with anti-tumor activity, extracted from patent WO2018027097A1. Bcl-2/Bcl-xl inhibitor 1 exhibits IC50 values of 2 nM and 5.9 nM for Bcl-2 and Bcl-xl, respectively[1].
PROTAC Bcl-xL degrader-3 is a potent ROTAC Bcl-xL degrader (WO2020163823A2, compound 44)[1].
Obatoclax (GX15-070), a BH3 mimetic, is a pan-BCL-2 family proteins inhibitor with a Ki of 220 nM for BCL-2[1][2]. Obatoclax induces autophagy-dependent cell death and targets cyclin D1 for proteasomal degradation. Obatoclax has anti-cancer and broad-spectrum antiparasitic activity[3][4].
Bcl-2-IN-10 is an active Bcl-2 inhibitor that can release up to four nitric oxide (NO) molecules. Bcl-2-IN-10 has cytotoxic activities against cancer cells, such as human leukemia, breast cancer and lung cancer. Bcl-2-IN-10 induces cell apopotosis and arrest cell cycle of G2/M phase, and can be used in cancer-related research[1].
Anticancer agent 65 (compound 4c) shows excellent activity in cancer cell lines, especially A549 cells, with an IC50 of 1.07 μM. Anticancer agent 65 induces S-phase arrest in A549 cells and increases the expression level of p53 and p21. Anticancer agent 65 causes apoptosis, ROS generation and collapse of MMP in A549 cells[1].
S55746 is an orally active, selective and potent BCL-2 inhibitor, with a Ki of 1.3 nM.
Thevetiaflavone could upregulate the expression of Bcl‑2 and downregulate that of Bax and caspase‑3.
Mcl1-IN-4 is an inhibitor of Mcl1 with an IC50 of 0.2 μM.
Mcl-1 inhibitor 8 is a MCL-1 inhibitor, example 228, extracted from patent WO2019222112[1].
Aspidin BB is a phloroglucinol derivative, which can be isolated from the aerial part of Dryopteris championii. Aspidin BB has anticancer activity. Aspidin BB induces cell cycle arrest and apoptosis in human ovarian HO-8910 cells[1][2].
Ginsenoside Rh4 is a rare saponin obtained from Panax notoginseng. Ginsenoside Rh4 activates Bax, caspase 3, caspase 8, and caspase 9. Ginsenoside Rh4 also induces autophagy.
Jaceosidin is a flavonoid isolated from Artemisia vestita, induces apoptosis in cancer cells, activates Bax and down-regulates Mcl-1 and c-FLIP expression[1]. Jaceosidin exhibits anti-cancer[2], anti-inflammatory activities, decreases leves of inflammatory markers, and suppresses COX-2 expression and NF-κB activation[3].