LXR-623

• CAT Number: I005274
• CAS Number: 875787-07-8
• Molecular Formula: C21H12ClF5N2
• Molecular Weight: 422.8
• Purity: ≥95%
• Synonyms: 2-[(2-chloro-4-fluorophenyl)methyl]-3-(4-fluorophenyl)-7-(trifluoromethyl)indazole
• Target: LXR
• Solubility: DMSO: ≥ 47 mg/mL
• Storage: room temp
• InChI: InChI=1S/C21H12ClF5N2/c22-18-10-15(24)9-6-13(18)11-29-20(12-4-7-14(23)8-5-12)16-2-1-3-17(19(16)28-29)21(25,26)27/h1-10H,11H2
• InChIKey: KYWWJENKIMRJBI-UHFFFAOYSA-N
• SMILES: C1=CC2=C(N(N=C2C(=C1)C(F)(F)F)CC3=C(C=C(C=C3)F)Cl)C4=CC=C(C=C4)F

LXR-623 (Cat No.: I005274) is a groundbreaking liver X-receptor (LXR) agonist, demonstrating impressive potency with IC50 values of 179 nM and 24 nM for LXR-α and LXR-β, respectively. This compound is biologically active when administered orally and possesses the unique ability to penetrate the blood-brain barrier. These qualities make LXR-623 a valuable tool for researchers exploring LXR-related pathways and potential therapeutic applications in various fields. For further details or specific inquiries regarding LXR-623, please do not hesitate to contact us.

Reference

1:J Clin Pharmacol. 2009 Jun;49(6):643-9. doi: 10.1177/0091270009335768. Epub 2009 Apr 27. Safety, pharmacokinetics, and pharmacodynamics of single doses of LXR-623, a novel liver X-receptor agonist, in healthy participants.Katz A,Udata C,Ott E,Hickey L,Burczynski ME,Burghart P,Vesterqvist O,Meng X, PMID: 19398602 DOI: 10.1177/0091270009335768
Abstract: Liver X-receptor (LXR) agonists have been postulated to enhance reverse cholesterol transport (RCT), a process believed to shuttle cholesterol from the periphery back to the liver. Enhancing RCT via the upregulation of cholesterol transporters such as the adenosine triphosphate-binding cassettes ABCA1 and ABCG1 could therefore inhibit the progression of atherosclerosis. LXR-623 is a synthetic ligand for LXRs alpha and beta that has shown promise in animal models of atherosclerosis. The authors present results from a single ascending-dose study of the safety, pharmacokinetics, and pharmacodynamics of LXR-623 in healthy participants. LXR-623 was absorbed rapidly with peak concentrations (C(max)) achieved at approximately 2 hours. The C(max) and area under the concentration-time curve increased in a dose-proportional manner. The mean terminal disposition half-life was between 41 and 43 hours independently of dose. LXR activation resulted in a dose-dependent increase in ABCA1 and ABCG1 expression. The effect of LXR-623 concentration on ABCA1 and ABCG1 expression was further characterized via a population pharmacokinetic-pharmacodynamic analysis, yielding EC(50) estimates of 526 ng/mL and 729 ng/mL, respectively. Central nervous system-related adverse events were observed at the 2 top doses tested. The pharmacodynamic effects described here are the first demonstration of /target engagement/ by an LXR agonist in humans.