etoposide

Etoposide (VP-16-213) is a topoisomerase II inhibitor that inhibits DNA synthesis by forming a complex with topoisomerase II and DNA (IC50=60.3 μM). Etoposide has antitumor activity and induces apoptosis and autophagy.

Etoposide phosphate disodium (BMY-40481 disodium), a phosphate ester prodrug of etoposide, is a potent chemotherapeutic agent that selectively inhibits topoisomerase II, hindering the re-ligation of DNA strands. Regarded as the active equivalent of etoposide, it effectively induces cell cycle arrest, apoptosis, and autophagy in cancer cells.

Apoptosis Inhibitor was a novel inhibitor of programmed cell death associate with caspase-3 inhibition.

Etoposide impurity 1 is an impurity associated with Etoposide.

Etoposide Phosphate is a selective and orally active topoisomerase II inhibitor and anticancer chemotherapy drug that inhibits cancer cell growth and induces apoptosis through DNA damage, the p53 pathway, and G2/M phase arrest of the cell cycle.

Etoposide-13C,D3 is a form of etoposide (TMSM-3462) that is labeled with 13C and deuterium. Etoposide (VP-16; VP-16-213) is a widely used antitumor chemotherapeutic agent. It functions by inhibiting topoisomerase II, thereby hindering DNA replication. Additionally, etoposide induces cell cycle arrest, apoptosis, and autophagy.

Etoposide (Standard) is a reference standard for research and analysis in studies involving Etoposide. Etoposide (VP-16-213) is a topoisomerase II inhibitor that inhibits DNA synthesis by forming a complex with topoisomerase II and DNA (IC50=60.3 μM). Etoposide has antitumor activity and induces apoptosis and autophagy.

Etoposide-[13C,D3] (Standard) is a reference standard of Etoposide-[13C,D3] intended for quantitative analysis, quality control, and related biochemical research applications.

ProTAME is an inhibitor of APC/CFzr and APC/CCdc20. Combinations of proTAME with topoisomerase inhibitors, doxorubicin and etoposide, significantly increase cell death in primary cells and Multiple Myeloma (MM) cell lines, particularly if TOPIIα levels are first increased through pre-treatment with ProTAME.This compound is unstable in powder form and other related salt forms are recommended.

Pifithrin-α, p-Nitro, Cyclic (PFN-α) is a cell-permeable, active-form inhibitor of p53.

BRD-K20733377 is a Bcl-2 inhibitor that exhibits selective cytotoxicity toward senescent cells, specifically inhibiting the activity of etoposide-induced senescent IMR-90 cells with an IC50 of 10.7 μM. Additionally, BRD-K20733377 reduces the mRNA expression of aging-related genes p16, p21, and KI67 in aged mouse models.

NecroX-2 is a cell-permeable necrosis inhibitor with antioxidant properties. NecroX-2 selectively suppresses necrotic cell death triggered by oxidative stress. NecroX-2 does not confer protection against apoptosis induced by staurosporine or etoposide but shows protective effects under conditions such as cold shock, hypoxia, and oxidative stress in vitro.

P-gp inhibitor 24 (Compound 10) is an inhibitor of P-glycoprotein (P-gp) that blocks P-gp-mediated efflux of fluorescent dyes. This compound is effective in reversing multidrug resistance (MDR) and can enhance the cytotoxic effects of Vincristine and Etoposide on cancer cells.

TMPO (3,3,5,5-Tetramethyl-1-pyrroline 1-oxide) is a spin-trapping agent that targets free radicals. It scavenges superoxide anions and hydroxyl radicals, and inhibits thymocyte apoptosis with an EC50 value of 19.1 mM for DNA fragmentation induced by MPS and 30.7 mM by Etoposide. TMPO reacts with intracellular free radicals to form stable nitroxide radical products, thereby reducing oxidative stress (such as lowering peroxide levels and maintaining glutathione content) and blocking oxidative events in the apoptosis pathway. TMPO shows potential for research in apoptosis of immune cells like thymocytes.

PNR-3-80 is a selective inhibitor of apoptotic endonuclease G (EndoG), with an IC50 of 0.67 μM, showing greater inhibition than against DNase I. It exhibits no inhibitory activity against DNase II, RNase A, proteases, lactate dehydrogenase, and superoxide dismutase 1. PNR-3-80 effectively protects human prostate cancer cells from cell death induced by Cisplatin and Docetaxel and inhibits DNA damage and autophagy (autophagy) prompted by Etoposide. This compound is applicable in studies of cellular damage.

HDAC1-IN-11 (Compound 6) is an HDAC1 inhibitor with an IC50 of 106.6 nM. It suppresses the expression of Sp1 and RAD51, leading to Caspase-dependent apoptosis. HDAC1-IN-11 exhibits antitumor activity and enhances the sensitivity of Etoposide and Gemcitabine by promoting synergistic cell death in NSCLC through inhibiting homologous recombination and non-homologous end joining (NHEJ) pathways involved in DNA double-strand break repair. It is applicable in chemotherapy research for cancers such as NSCLC.

HDAC6-IN-63 (Compound 7) is an orally active inhibitor of HDAC6 with an IC50 of 145 nM. It suppresses the expression of Sp1 and RAD51, inducing caspase-dependent apoptosis. HDAC6-IN-63 exhibits antitumor activity and enhances the sensitivity of Etoposide and Gemcitabine by inhibiting homologous recombination and non-homologous end joining (NHEJ) pathways involved in DNA double-strand break (DSB) repair, promoting synergistic cell death in NSCLC cells. This compound is applicable for chemotherapy research in cancers such as NSCLC.

MS-073 (CP-162398) is a P-glycoprotein inhibitor (P-gp). The in vitro resistance to vincristine (VCR) was almost completely reversed in VCR-resistant P388 cells, and the resistance of VCR, adriamycin (ADM), etoposide, and actinomycin D in ADM-resistant hu

NK 611 is a new semisynthetic analogue of etoposide and has been found to be more potent against several cancer cell lines in vitro than etoposide.

NSC 660028 is a novel γ-lactone ring modified arylamino etoposide analogram with strong antitumor activity as an inhibitor of human DNA topoisomerase II.

10'-Desmethoxystreptonigrin is an antibiotic originally isolated from Streptomyces and a derivative of the antibiotic streptonigrin. It is active against a variety of bacteria, including S. aureus, S. faecalis, E. coli, K. pneumoniae, and P. vulgaris (MICs = 0.4, 1.6, 3.1, 3.1 and 0.4 μg/ml, respectively). 10'-Desmethoxystreptonigrin is cytotoxic to HCT116 colon and A2780 ovarian cancer cells (IC50s = 0.004 and 0.001 μg/ml, respectively), as well as HCT116 cells resistant to etoposide and teniposide and cisplatin-resistant A2780 cells (IC50s = 0.003, 0.001, and 0.01 μg/ml, respectively). 10'-Desmethoxystreptonigrin is also an inhibitor of p21ras farnesylation (IC50 = 21 nM).

Potent Chk2 inhibitor (IC50 = 3 nM). Shows >63-fold selectivity for Chk1 over Chk2 and a panel of 84 other kinases. Inhibits Chk2 activation in response to etoposide-induced DNA damage in HT29 cells. Blocks ionizing radiation-induced apoptosis of mouse thymocytes. Caldwell et al (2011) Structure-based design of potent and selective 2-(quinazolin-2-yl)phenol inhibitors of checkpoint kinase 2. J.Med.Chem. 54 580 PMID:21186793

ARN-21934 is a potent, highly selective, blood-brain barrier (BBB) penetrant inhibitor for human topoisomerase II α over β. It inhibits DNA relaxation with an IC50 of 2 μM, compared to 120 μM for Etoposide. ARN-21934 exhibits favorable in vivo pharmacokinetic properties and shows promise in anticancer research, displaying affinity for topoIIα with an IC50 of 2 μM and for topoIIβ with an IC50 of 120 μM. It demonstrates activity against human cancer cell lines including melanoma (A375: 12.6 μM, G-361: 8.1 μM), breast (MCF7: 15.8 μM), endometrial (HeLa: 38.2 μM), lung (A549: 17.1 μM), and prostate (DU145: 11.5 μM) cancer cells. Following a single intraperitoneal injection of 10 mg/kg, ARN-21934 achieves a peak plasma concentration of 0.68 μg/mL in 15 minutes, with a half-life of 149 minutes, and remains detectable in plasma and the brain for up to 360 minutes. [1] Jose Antonio Ortega, et al. Novel, Potent, and Druglike Tetrahydroquinazoline Inhibitor That Is Highly Selective for Human Topoisomerase II α over β. J Med Chem. 2020 Nov 12;63(21):12873-12886.

Heptelidic acid (Koningic acid) is a sesquiterpenoid lactone antibiotic derived from the probiotic fungus Aspergillus oryzae, a selective GAPDH inhibitor. It downregulates caspase to inhibit etoposide-induced apoptosis. Heptelidic acid inhibits tau fibrillation in a concentration-dependent manner and exerts antitumor effects on extra-intestinal melanoma by controlling glyceraldehyde-3-phosphate dehydrogenase activity.