Ly101-4B 

Ly101-4B is an apoptosis inducer and multi-target inhibitor with antiproliferative, antitumor and cycytotoxic effects. Ly101-4B reduces HSF1 expression, inhibits microRNA-214 synthesis, downregulates HSP27, HSP70 and HSP90 expression, while suppressing E2F-dependent transcriptional activity and downregulating its target genes. Ly101-4B induces caspase 3/7-mediated apoptosis by reducing DNA synthesis, inhibiting the cell cycle and G1/S phase transition, without affecting RNA synthesis or inducing necrosis. Ly101-4B is selective for pancreatic ductal adenocarcinoma cells with different genotypes and varying degrees of E2F dependence. Ly101-4B can be used in research related to epithelial ovarian cancer and pancreatic ductal adenocarcinoma^[1][2][3].

Ly101-4B (20-100 μM; 24-48 h) inhibits the proliferation of human epithelial cisplatin-resistant ovarian cancer cell line SKOV3, induces its apoptosis, and downregulates the expression of HSF1, HSP27, HSP70 and HSP90 in these cells^[1].
Ly101-4b (20-100 μM; 48 h) reduces the viability of primary Nupr1-deficient and Nupr1 wt; KIC pancreatic cancer cells, and exerts a significantly differential effect at the concentration of 100 μM^[2].
Ly101-4B (1-25 μM; 12-72 h) inhibits E2F activity in MiaPaCa2 cells in luciferase activity assays using E2F-dependent reporter gene vectors^[3].
Ly101-4B (25 μM; 12-72 h) reduces the viability of MiaPaCa2 cells, induces caspase 3/7-mediated apoptosis, and inhibits DNA synthesis, without affecting RNA synthesis or triggering necrosis^[3].
Ly101-4B exhibits greater potency against primary PDAC cells with high E2F expression (CRCM93, CRCM08, CRCM17) than against those with low E2F expression (CRCM10, CRCM12, CRCM110, CRCM92), with a lower 72 h IC₅₀ value (19.4 μM vs 44.1 μM)^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Ly101-4B (100 mg/kg; i.p.; twice weekly for 4 consecutive weeks) significantly inhibits the in vivo growth of ovarian tumors in female nude mice (athymic mice) by downregulating HSF1 and miR-214, with no adverse effects^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

442.51

C₂₃H₃₀N₄O₅

1415728-94-7

O[C@H]1[C@@H](O)[C@H](N2C(C(N)=O)=NC(C#CC3=CC=C(CCCCCCC)C=C3)=N2)O[C@@H]1CO

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Chen YF, et al. Nucleoside analog inhibits microRNA-214 through targeting heat-shock factor 1 in human epithelial ovarian cancer. Cancer Sci. 2013;104(12):1683-1689.  [Content Brief]

  [2]. Cano CE, et al. Genetic inactivation of Nupr1 acts as a dominant suppressor event in a two-hit model of pancreatic carcinogenesis. Gut. 2014;63(6):984-995.  [Content Brief]

  [3]. Lan W, et al. E2F signature is predictive for the pancreatic adenocarcinoma clinical outcome and sensitivity to E2F inhibitors, but not for the response to cytotoxic-based treatments. Sci Rep. 2018;8(1):8330. Published 2018 May 29.  [Content Brief]