Survivin

Sepantronium bromide (YM155) is a small-molecule proapoptotic agent with potential antineoplastic activity.

Patritumab (U3-1287) is an anti-HER3 monoclonal antibody with potential antitumor activity and inhibits phosphorylation of EGFR, HER2, HER3, ERK, and AKT.Patritumab promotes apoptosis and inhibits proliferation in non-small cell lung cancer.

Shepherdin 79-87 acetate is a peptidomimetic antagonist of the complex between Hsp90 and survivin, another key regulator of tumor cell viability.

Isolinderalactone shows anti-inflammatory and anticancer capacity, and it exhibits moderate iNOS inhibitory activity, with the IC50 value of 0.30 uM.

FL118 is a novel survivin inhibitor that inhibits cancer stem cell-like properties.FL118 is a novel camptothecin analog with anticancer activity that inhibits epithelial-mesenchymal transition through the Wnt β-catenin signaling pathway, thereby inhibiting migration and invasion of human breast cancer cells.

1. Cucurbitacin IIA (Dihydrocucurbitacin Q1) can induce apoptosis and enhance autophagy , contributes to the anti-inflammatory activity of Cucurbitacin IIA against inflammation-related diseases. 2. Cucurbitacin IIA is a novel class of anti-cancer drug in suppression of cancer cell expansion by disrupting the actin cytoskeleton and directing the cell to undergo PARP-mediated apoptosis through the inhibition of survivin downstream of JAK2 STAT3.

GDP366, a dual inhibitor of survivin and Op18, induces cell growth inhibition, cellular senescence, and mitotic catastrophe in human cancer cells.

MNK8 (3-methyl-6-(naphthalen-1-yl)pyrimidine-2,4(1H,3H)-dione) is a potent STAT3 inhibitor that reduces the ability of STAT3 to bind to DNA and also has a good growth inhibition effect on liver cancer cells [1].

Levonorgestrel (D-Norgestrel) is a Progestin and Progestin-containing Intrauterine Device. The physiologic effect of levonorgestrel is by means of Inhibit Ovum Fertilization.

2,5-dimethyl Celecoxib is a derivative of celecoxib that does not inhibit COX-2 (IC50 = >100 μM).1 It does inhibit microsomal prostaglandin E synthase-1 (mPGES-1) in HeLa cells (IC50 = 15.6 μM) and reduces prostaglandin E2 production in HeLa, A549, and HCA-7 cells (IC50s = 0.64, 0.83, and 3.08 μM, respectively).2 It inhibits proliferation of drug-sensitive RPMI8226 and multidrug-resistant 8226/Dox40 multiple myeloma cells, as well as increases the rate of apoptosis when used at concentrations of 20 and 30 μM.3 2,5-dimethyl Celecoxib reduces the expression of survivin, cyclin A, cyclin B, MEK1, and MEK2 in 8226/Dox40 cells. The antiproliferative effect of 2,5-dimethyl celecoxib is independent of mPGES-1 inhibition.2References1. Zhu, J., Song, X., Lin, H.-P., et al. Using cyclooxygenase-2 inhibitors as molecular platforms to develop a new class of apoptosis-inducing agents. J. Natl. Cancer Inst. 94(23), 1745-1757 (2002).2. Wobst, I., Schiffmann, S., Birod, K., et al. Dimethylcelecoxib inhibits prostaglandin E2 production. Biochem. Pharmacol. 76(1), 62-69 (2008).3. Kardosh, A., Soriano, N., Liu, Y.-T., et al. Multitarget inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib (DMC), a non-COX-2 inhibitory analog of celecoxib. Blood 106(13), 4330-4338 (2005). 2,5-dimethyl Celecoxib is a derivative of celecoxib that does not inhibit COX-2 (IC50 = >100 μM).1 It does inhibit microsomal prostaglandin E synthase-1 (mPGES-1) in HeLa cells (IC50 = 15.6 μM) and reduces prostaglandin E2 production in HeLa, A549, and HCA-7 cells (IC50s = 0.64, 0.83, and 3.08 μM, respectively).2 It inhibits proliferation of drug-sensitive RPMI8226 and multidrug-resistant 8226/Dox40 multiple myeloma cells, as well as increases the rate of apoptosis when used at concentrations of 20 and 30 μM.3 2,5-dimethyl Celecoxib reduces the expression of survivin, cyclin A, cyclin B, MEK1, and MEK2 in 8226/Dox40 cells. The antiproliferative effect of 2,5-dimethyl celecoxib is independent of mPGES-1 inhibition.2 References1. Zhu, J., Song, X., Lin, H.-P., et al. Using cyclooxygenase-2 inhibitors as molecular platforms to develop a new class of apoptosis-inducing agents. J. Natl. Cancer Inst. 94(23), 1745-1757 (2002).2. Wobst, I., Schiffmann, S., Birod, K., et al. Dimethylcelecoxib inhibits prostaglandin E2 production. Biochem. Pharmacol. 76(1), 62-69 (2008).3. Kardosh, A., Soriano, N., Liu, Y.-T., et al. Multitarget inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib (DMC), a non-COX-2 inhibitory analog of celecoxib. Blood 106(13), 4330-4338 (2005).

Proadifen hydrochloride (RP-5171) is an inhibitor of drug metabolism and cytochrome P-450 enzyme system activity.

LQZ-7I is an inhibitor of surviving-targeting. It orally effectively inhibits xenograft tumor growth and induces survivin loss in tumors

LQZ-7F is a small molecule survivin dimerisation inhibitor with anticancer activity.LQZ-7F induces proteasome-dependent survivin degradation, mitotic arrest, and apoptosis, and blocks human tumour growth in mouse xenograft assays.

YAP TAZ-TEAD-IN-2 (Compound 51) is a YAP TAZ-TEAD inhibitor that disrupts the interaction between YAP TAZ and TEAD. It inhibits the transcriptional activity of TEAD with an IC50 of 1.2 nM. Additionally, YAP TAZ-TEAD-IN-2 suppresses the expression of target genes (Cyr61, CTGF, AXL, and Survivin) and the proliferation of breast cancer cells.

Shepherdin 79-87, comprising amino acids 79 to 87 of Shepherdin, acts as a peptidomimetic antagonist targeting the Hsp90-Survivin complex, exhibiting anticancer properties.

Survivin (also known as baculoviral IAP repeat-containing protein 5 (BIRC5)) is a member of the inhibitor of apoptosis (IAP) family that interacts with and inhibits the apoptotic function of several proteins. LLP-3 is a cell-permeable ligand of Survivin that blocks its interaction with Ran, resulting in the induction of apoptosis (IAP) in glioma stem cells (IC50 = 31 μM). It abolishes the growth of glioblastoma multiforme cell in spheres and in tumor slice cultures.

Sepantronium hydrochloride (YM-155 hydrochloride) is a novel survivin suppressant that inhibits the survivin promoter with an IC₅₀ of 0.54 nM[1].

K882 (Compound 4e) is an Src inhibitor with a KD of 0.315 μM. It induces apoptosis and inhibits XIAP and Survivin. Additionally, K882 blocks the activation of the PI3K/Akt/mTOR, Jak1/Stat3, and Ras/MAPK signaling pathways. K882 exhibits antitumor activity against non-small cell lung cancer.

HVH-2930 is an inhibitor of Heat Shock Protein 90 (HSP90). It suppresses the cell viability of BT474 (Trastuzumab sensitive) and JIMT-1 (Trastuzumab resistant) by downregulating HSP90 client proteins such as HER2, p-HER2, AKT, p-AKT, cyclin D1, and survivin, with IC50 values of 6.86 μM and 4.42 μM, respectively. Additionally, HVH-2930 demonstrates antitumor efficacy in a mouse model and exhibits favorable pharmacokinetic properties in vivo.

LFS-1107, a reversible CRM1 inhibitor (Kd: 12.5 pM), selectively targets and eliminates ENKTL cells, offering potential for cancer research applications [1].

MX107 is a survivin inhibitor which induces degradation of XIAP and or cIAP1, and suppresses genotoxic NF-kappaB activation.

AQIM-I is a survivin inhibitor that reduces survivin expression and colony formation. It promotes reactive oxygen species (ROS) production, apoptosis, cell cycle arrest, DNA damage, and autophagy. Moreover, AQIM-I effectively inhibits nonsmall cell lung cancer cells A549, with an IC 50 value of 9 nM [1].