Anticancer agent 56 (compound 4d) is a potent anti-cancer agent with drug-likeness properties, possessing anticancer activity against several cancer cell lines (IC50<3 μM). Anticancer agent 56 induces cell cycle arrest at G2/M phase and triggers mitochondrial apoptosis pathway. Anticancer agent 56 acts by accumulation of ROS, up regulation of BAX, down regulation of Bcl-2 and activation of caspases 3, 7, 9[1].
NWP-0476 is BCL-2/BCL-xL inhibitor. NWP-0476 has a modified structure with fine-tuned BCL-xL activity. NWP-0476 can be used for relapsed T-acute lymphoblastic leukemia (T-ALL) research[1].
Venetoclax-d8 is deuterium labeled Venetoclax. Venetoclax (ABT-199; GDC-0199) is a highly potent, selective and orally bioavailable Bcl-2 inhibitor with a Ki of less than 0.01 nM. Venetoclax induces autophagy[1][2][3].
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].
TC11 is a MCL1 degradator and Caspase-9 and CDK1 activator. TC11 structurally relates to immunomodulatory drugs as phenylphthalimide derivative. TC11 induces apoptotic death caused by degradation of MCL1 during prolonged mitotic arrest[1][2].
Mcl1-IN-8 (Comp8) is a Mcl-1-PUMA interface inhibitor, with a Ki of 0.3 μM. Mcl1-IN-8 (Comp8) exhibits dual activity on reduce PUMA-dependent apoptosis while deactivating Mcl-1-mediated anti-apoptosis in cancer cells[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].
Estrogen receptor modulator 10 (compound G-5b) is an Estrogen receptor (ER) antagonist (IC50=6.7 nM) and degrader (DC50=0.4 nM). Estrogen receptor modulator 10 can induce apoptosis. Estrogen receptor modulator 10 can block cells at the G1/G0 phase. Estrogen receptor modulator 10 can be used in cancer studies[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].
Obatoclax is an antagonist of the BCL-2 family proteins. It binds to BCL-2 with a Ki of 220 nM.
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].
(R)-(-)-Gossypol acetic acid (AT-101 (acetic acid)) is the levorotatory isomer of a natural product Gossypol. AT-101 is determined to bind to Bcl-2, Mcl-1 and Bcl-xL proteins with Kis of 260±30 nM, 170±10 nM, and 480±40 nM, respectively.
S65487 (VOB560) hydrochloride is a potent and selective Bcl-2 inhibitor. S65487 hydrochloride is also active on BCL-2 mutations, such as G101V and D103Y. S65487 hydrochloride has poor affinity with MCL-1, BFL-1 and BCL-XL. S65487 hydrochloride induces apoptosis and has anticaner activities[1][2].
Anticancer Agent 43 is a potent anticancer agent. Anticancer Agent 43 induces apoptosis by caspase 3, PARP1, and Bax dependent mechanisms. Anticancer Agent 43 induces DNA damage[1].
Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling[1][2][3].
8α-Tigloyloxyhirsutinolide 13-O-acetate is a potent and orally active STAT3 inhibitor. 8α-Tigloyloxyhirsutinolide 13-O-acetate induces early oxidative stress and Pyroptosis, and late DNA damage, cell cycle arrest, Apoptosis in the TNBC cells. 8α-Tigloyloxyhirsutinolide 13-O-acetate suppresses tumor cell growth in vitro and tumor growth in vivo[1][2].
BCL6-IN-3 (example 20a) is a B-cell lymphoma 6 (BCL6) inhibitor with anti-tumor activity, extracted from patent WO2018215801A1. BCL6-IN-3 (example 20a) exhibits a GI50 of 70 nM in SU-DHL4 cells[1].
Dehydrobruceine B, a quassinoid, can be isolated from Brucea javanica. Dehydrobruceine B shows a synergistic effect with Cisplatin (HY-17394) to induce apoptosis via mitochondrial method. Dehydrobruceine B increases apoptosis-inducing factor (AIF) and Bax expression and suppresses Keap1-Nrf2[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].
Mcl-1 inhibitor 3 (compound 1) is a highly potent and orally activate macrocyclic Mcl-1 inhibitor (Ki= 0.061 nM; IC50=19 nM in an OPM-2 cell viability assay). Mcl-1 inhibitor 3 shows good pharmacokinetic properties and excellent in vivo efficacy without toxicity[1]. .
Antitumor agent-55 (compound 5q) is a potent antitumor agent. Antitumor agent-55 effectively inhibits PC3, with an IC50 of 0.91 μM. Antitumor agent-55 effectively inhibits the colony formation, suppresses the cell migration in PC3. Antitumor agent-55 induces G1/S phase arrest and apoptosis in PC3[1].
KRN5500 (NSC 650426), a Spicamycin (HY-127130) derivative and a nucleoside-like antibiotic with anti-tumor activity. KRN5500 also induces apoptosis via the down-regulation of Bcl-2 expression. KRN5500 shows a significant efficacy in the human tumor xenograft model in mice[1][2].
Hrk BH3 is a biological active peptide. (BH3 domain of Hrk)
Clezutoclax is a potent payload and also a Bcl-XL inhibitor. Clezutoclax can be used in the synthesis of antibody-drug conjugates (ADCs)[1].
dMCL1-2 is a potent and selective degrader of myeloid cell leukemia 1 (MCL1) based on PROTAC, which binds to MCL1 with a KD of 30 nM. dMCL1-2 activats the cellular apoptosis machinery by degradation of MCL1[1].
Sonrotoclax is a potent, orally active Bcl2 inhibitor. Sonrotoclax has effective cell killing effect against a variety of lymphoma and leukemia cell lines[1].
TCPOBOP is a constitutive androstane receptor (CAR) agonist that induces robust hepatocyte proliferation and hepatomegaly without any liver injury or tissue loss[1]. TCPOBOP attenuates Fas-induced murine liver injury by altering Bcl-2 proteins[2].