Escin IA

Escin IA is an oral LOXL2 inhibitor and EMT inhibitor, with selectivity for LOXL2-expressing cells. Escin IA suppresses invasion, migration, and metastasis of breast cancer cells, and acts as the primary anti-TNBC metastasis constituent of Aesculus chinensis Bunge fruit saponin fraction. Escin IA can be used for the research of triple-negative breast cancer, acute inflammation, and ethanol-induced gastric mucosal lesions^[1][2][3][4]. In Vitro:Escin Ia (2.5-10 μM; 24 h) inhibits the invasion of MDA-MB-231 cells in a concentration-dependent manner, with 10 μM causing the highest inhibition (76.23%)^[1].
Escin Ia (2.5-10 μM; 24 h) modulates mRNA expression of LOXL2, E-cadherin, and MMP9 in MDA-MB-231 cells, with LOXL2 down-regulation and E-cadherin up-regulation being prominent effects^[1].
Escin Ia (2.5-10 μM; 6-24 h, unspecified intervals) suppresses the epithelial-mesenchymal transition (EMT) process in MDA-MB-231 cells by modulating EMT markers and transcription factors^[1].
Escin Ia (2.5-10 μM; 6-24 h, unspecified intervals) reverses the EMT process in TNF−α/TGF−β-stimulated MCF-7 cells by normalizing EMT marker expressions^[1].
Escin Ia (2.5-10 μM; 6-24 h, unspecified intervals) down-regulates LOXL2 expression in MDA-MB-231 cells and abrogates induced LOXL2 expression in TNF-α/TGF-β-stimulated or LOXL2-transfected MCF-7 cells^[1].
Escin Ia (2.5-10 μM; unspecified intervals) inhibits the EMT process in LOXL2-transfected MCF-7 cells by down-regulating LOXL2 and normalizing EMT markers^[1].
Escin Ia (2.5-10 μM; unspecified intervals) inhibits the EMT process in hypoxia-stimulated MCF-7 cells by down-regulating LOXL2 (without affecting HIF-1α) and normalizing EMT markers^[1]. In Vivo:Escin Ia (2-4 mg/kg; i.p.; three times per week; five weeks) suppresses TNBC metastasis and EMT in MDA-MB-231 xenograft mice by down-regulating LOXL2, with 4 mg/kg showing greater efficacy than 2 mg/kg^[1].
Escin Ia (50-200 mg/kg; p.o.) dose-dependently inhibits acetic acid-induced vascular permeability in Mus musculus, with 43.6% inhibition at 200 mg/kg^[2].
Escin Ia (25-200 mg/kg; p.o.) inhibits compound 48/80-induced scratching in mice, with significant 42.4% inhibition at 200 mg/kg^[2].
Escin Ia (200 mg/kg; p.o.) significantly inhibits the early phase (1 hour) of carrageenin-induced hind paw edema in rats^[2].
Escin Ia (25-200 mg/kg; p.o.) dose-dependently inhibits histamine-induced vascular permeability in rats (significant at 50-200 mg/kg) but does not inhibit serotonin-induced vascular permeability^[2].
Escin IA (10-50 mg/kg; p.o.; single dose 1 hour before ethanol administration) potently protects against ethanol-induced gastric mucosal lesions in rats via mechanisms involving capsaicin-sensitive afferent neurons, endogenous nitric oxide, and prostaglandins, with no gastric antisecretory activity at effective doses^[4].
Escin IA (10 mg/kg; p.o.; single dose 1 hour before ethanol administration) relies on capsaicin-sensitive afferent neurons for its gastroprotective effect in rats^[4].
Escin IA (10 mg/kg; p.o.; single dose 1 hour before ethanol administration) relies on endogenous prostaglandins for its gastroprotective effect in rats^[4].
Escin IA (10 mg/kg; p.o.; single dose 1 hour before ethanol administration) relies on endogenous nitric oxide for its gastroprotective effect in rats^[4].
Escin IA (10 mg/kg; p.o.; single dose 1 hour before ethanol administration) does not rely on endogenous sulfhydryls for its gastroprotective effect in rats^[4].
Escin IA (10-20 mg/kg; p.o.; single dose 1 hour before ethanol administration) relies on the sympathetic nervous system for its gastroprotective effect in rats^[4].