ERX-41

• CAT Number: I041978
• CAS Number: 2440087-54-5
• Molecular Formula: C38H48N4O9
• Molecular Weight: 704.81
• Purity: ≥95%
• Synonyms: 4-[[4-[[3-(2-hydroxyethoxy)-4-nitrobenzoyl]amino]-3-(2-methylpropoxy)benzoyl]amino]-N-(4-methylcyclohexyl)-3-(2-methylpropoxy)benzamide
• InChI: InChI=1S/C38H48N4O9/c1-23(2)21-50-33-18-26(36(44)39-29-11-6-25(5)7-12-29)8-13-30(33)40-37(45)27-9-14-31(34(19-27)51-22-24(3)4)41-38(46)28-10-15-32(42(47)48)35(20-28)49-17-16-43/h8-10,13-15,18-20,23-25,29,43H,6-7,11-12,16-17,21-22H2,1-5H3,(H,39,44)(H,40,45)(H,41,46)
• InChIKey: QOYORXKDWMJNHD-UHFFFAOYSA-N
• SMILES: CC1CCC(CC1)NC(=O)C2=CC(=C(C=C2)NC(=O)C3=CC(=C(C=C3)NC(=O)C4=CC(=C(C=C4)[N+](=O)[O-])OCCO)OCC(C)C)OCC(C)C

ERX-41 is an orally active and stereospecific small molecule targeting to lysosomal acid lipase A (LIPA). ERX-41 induces endoplasmic reticulum (ER) stress resulting in cell death, indicating a function independent of LIPA but dependent on its ER localization. ERX-41 involves in a targeted strategy for solid tumors[1].
ERX-41 (1 μM; 0-30 h) induces cell death in MDA-MB-231 without significant effect against normal human mammary epithelial cells (HMECs)[1].
ERX-41 (1 μM; 2 h and 4 h) induces dramatic ER dilation within 4 h, and results disorganization of the peripheral ER network within 2 h[1].
ERX-41 (1 μM; 0.5-4 h) induces downstream unfolded protein response (UPR) pathways via induction of phosphorylated protein kinase R-like ER kinase (p-PERK) and phosphorylated eukaryotic translation initiation factor 2 subunit 1 (p-eIF2-α), and by expression of CCAAT-enhancer-binding homologous protein (CHOP) and phosphorylated inositol-requiring enzyme 1-α (IRE1-α) in TNBC[1].
ERX-41 (10 mg/kg; p.o. or i.p.; single dose) is detectable within 1.5 h in established s.c. MDA-MB-231 xenografts after either PO or i.p. administration[1].
ERX-41 (10 mg/kg; p.o.; single dose) significantly inhibits the progression without changing body weight in mouse model with MDA-MB-231 xenografts[1].
ERX-41 (10 mg/kg; p.o. or i.p.; single dose) significantly inhibits the progression in mouse model with MDA-MB-231 s.c. xenografts[1].

Reference

[1]. Liu X, et al. Targeting LIPA independent of its lipase activity is a therapeutic strategy in solid tumors via induction of endoplasmic reticulum stress. Nat Cancer. 2022 Jul;3(7):866-884.
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