161172-51-6
161172-51-6
Chemical Structure
Etalocib
Synonym(s): LY293111; VML 295
- CAS No.: 161172-51-6
- Formula:C33H33FO6
- Molecular Weight:544.61
IUPAC Name: 2-(3-(3-((5-ethyl-4'-fluoro-2-hydroxy-[1,1'-biphenyl]-4-yl)oxy)propoxy)-2-propylphenoxy)benzoic acid
InChIKey: YFIZRWPXUYFCSN-UHFFFAOYSA-N
SMILES: O=C(O)C1=CC=CC=C1OC2=CC=CC(OCCCOC3=C(CC)C=C(C4=CC=C(F)C=C4)C(O)=C3)=C2CCC
Biological Activity: Etalocib (LY293111), an orally active leukotriene B4 receptor antagonist, inhibits the binding of [3H]LTB4, with a Ki of 25 nM. Etalocib (LY293111) prevents LTB4-induced calcium mobilization with an lC50 of 20 nM. Etalocib (LY293111) induces apoptosis[1][2][3].
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Etalocib | 99.03% | Etalocib (LY293111), an orally active leukotriene B4 receptor antagonist, inhibits the binding of [3H]LTB4, with a Ki of 25 nM. Etalocib (LY293111) prevents LTB4-induced calcium mobilization with an lC50 of 20 nM. Etalocib (LY293111) induces apoptosis. | ||||||||||||||||||||
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Etalocib (Standard) | ≥98% | Etalocib (Standard) is the analytical standard of Etalocib. This product is intended for research and analytical applications. Etalocib (LY293111), an orally active leukotriene B4 receptor antagonist, inhibits the binding of [3H]LTB4, with a Ki of 25 nM. Etalocib (LY293111) prevents LTB4-induced calcium mobilization with an lC50 of 20 nM. Etalocib (LY293111) induces apoptosis. | ||||||||||||||||||||
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References
- [1]. P Marder, et al. Blockade of Human Neutrophil Activation by 2-[2-propyl-3-[3-[2-ethyl-4-(4-fluorophenyl)-5- Hydroxyphenoxy]propoxy]phenoxy]benzoic Acid (LY293111), a Novel Leukotriene B4 Receptor Antagonist. Biochem Pharmacol. 1995 May 26;49(11):1683-90. [Content Brief]
- [2]. S A Silbaugh, et al. Pharmacologic Actions of the Second Generation Leukotriene B4 Receptor Antagonist LY29311: In Vivo Pulmonary Studies. Naunyn Schmiedebergs Arch Pharmacol. 2000 Apr;361(4):397-404. [Content Brief]
- [3]. Wei-Gang Tong, et al. Leukotriene B4 Receptor Antagonist LY293111 Inhibits Proliferation and Induces Apoptosis in Human Pancreatic Cancer Cells. Clin Cancer Res. 2002 Oct;8(10):3232-42. [Content Brief]
