1202208-36-3

1202208-36-3 structure

Name: CAY10614
Chemical Name: cyclopentyl-[[3,4-di(tetradecoxy)phenyl]methyl]-dimethylazanium,iodide
CAS Number: 1202208-36-3
Molecular Formula: C₄₂H₇₈INO₂
Molecular Weight: 755.979
Catalog: Signaling Pathways Immunology/Inflammation Toll-like Receptor (TLR)
Create Date: 2017-01-23 13:55:44
Modify Date: 2024-04-05 06:15:28
CAY10614 is a potent TLR4 antagonist. CAY10614 inhibits the lipid A-induced activation of TLR4, with an IC50 of 1.675 μM. CAY10614 can improve survival of mice in lethal endotoxin shock model[1][2].

Name	cyclopentyl-[[3,4-di(tetradecoxy)phenyl]methyl]-dimethylazanium,iodide
Synonyms	Benzenemethanaminium, N-cyclopentyl-N,N-dimethyl-3,4-bis(tetradecyloxy)-, iodide (1:1) N-[3,4-Bis(tetradecyloxy)benzyl]-N,N-dimethylcyclopentanaminium iodide

Description	CAY10614 is a potent TLR4 antagonist. CAY10614 inhibits the lipid A-induced activation of TLR4, with an IC50 of 1.675 μM. CAY10614 can improve survival of mice in lethal endotoxin shock model[1][2].
Related Catalog	Signaling Pathways >> Immunology/Inflammation >> Toll-like Receptor (TLR) Research Areas >> Neurological Disease
Target	TLR4:1.675 μM (IC50, in HEK293 cells)
In Vitro	CAY10614 (compound 7) (1-10 μM) inhibits the lipid A-induced increase of phosphatase activity in a concentration-dependent manner in HEK293 cells[1]. CAY10614 (0.5 μM) inhibits the increase of [Ca2+]cyt induced by LPS in >18 days in vitro (DIV) neurons[2].
In Vivo	CAY10614 (compound 7) (10 mg/kg; i.p. 30 min before the LPS) significantly improves survival of mice given intraperitoneal LPS (20 mg/kg)[1]. Animal Model: C57BL/6J male mice (9 weeks) were i.p. injected with 20 mg/kg LPS[1] Dosage: 10 mg/kg Administration: I.p. 30 min before the LPS Result: Increased the survival rate of mice from 0% to 67%.
References	[1]. Piazza M, et, al. Glycolipids and benzylammonium lipids as novel antisepsis agents: synthesis and biological characterization. J Med Chem. 2009 Feb 26;52(4):1209-13. [2]. Rodríguez MC, et, al. Aging and amyloid β oligomers enhance TLR4 expression, LPS-induced Ca 2+ responses, and neuron cell death in cultured rat hippocampal neurons. J Neuroinflammation. 2017 Jan 31;14(1):24.