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161172-51-6

161172-51-6 structure
161172-51-6 structure
  • Name: LY293111
  • Chemical Name: Etalocib
  • CAS Number: 161172-51-6
  • Molecular Formula: C33H33FO6
  • Molecular Weight: 544.610
  • Catalog: Signaling Pathways Apoptosis Apoptosis
  • Create Date: 2017-06-29 04:36:23
  • Modify Date: 2025-08-24 18:13:57
  • 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].

Name Etalocib
Synonyms 2-(3-{3-[(5-Ethyl-4'-fluoro-2-hydroxy-4-biphenylyl)oxy]propoxy}-2-propylphenoxy)benzoic acid
LY293111
2-(3-{3-[(5-ethyl-4'-fluoro-2-hydroxybiphenyl-4-yl)oxy]propoxy}-2-propylphenoxy)benzoic acid
Etalocib
Benzoic acid, 2-[3-[3-[(5-ethyl-4'-fluoro-2-hydroxy[1,1'-biphenyl]-4-yl)oxy]propoxy]-2-propylphenoxy]-
LY-193111
Description 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].
Related Catalog
In Vitro Etalocib (LY293111) elicits a concentration-dependent inhibition of LTB4 induced CD11b up-regulation[1]. Etalocib (LY293111) is an extremely potent and selective antagonist of human neutrophil function in vitro[2]. Etalocib (LY293111, 250 and 500 nM, 24-72 h) induces apoptosis and inhibits proliferation in human pancreatic cancer cells[3]. Cell Proliferation Assay[3] Cell Line: MiaPaCa-2 and AsPC-1 human pancreatic cancer cells.[3] Concentration: 500 nM. Incubation Time: 24, 48, and 72 h. Result: Caused both a concentration-dependent and time-dependent inhibition of thymidine incorporation in both MiaPaCa-2 and AsPC-1 human pancreatic cancer cells. Apoptosis Analysis[3] Cell Line: MiaPaCa-2 and AsPC-1 human pancreatic cancer cells. Concentration: 250 and 500 nM. Incubation Time: 24 h. Result: Induced apoptosis in human pancreatic cancer cells.
In Vivo Etalocib (LY293111) produces a dose-related inhibition of acute leukotriene B4-induced airway obstruction when administered i.v. (ED50=14 µg/kg) or p.o. (ED50=0.4 mg/kg)[2]. Etalocib (LY293111, 10 mg/kg) inhibits A23187-induced lung inflammatory changes at 1 h[2]. Etalocib (LY293111, 250 mg/kg/day, orally) inhibits growth of human pancreatic cancer xenografts in athymic mice[3]. Animal Model: Guinea pigs[2]. Dosage: 1-10 mg/kg. Administration: Orally once. Result: A single 1 mg/kg oral dose inhibited excised lung gas volume increases by 76.7±7.1% (n=4, P<0.002) when given 8 h prior to leukotriene B4 challenge, and 28.6±20.3% (n=4, NS) when given 24 h before challenge. Had no effect (10 mg/kg) on pulmonary gas trapping at 1 h or 2 h after A23187 challenge. However, at 4 h, the pulmonary gas trapping response was significantly less than that of vehicle-treated controls and not different from sham values. The 10 mg/kg dose inhibited A23187-induced lung inflammatory changes at 1 h, but was without effect at 2 h or 4 h after challenge.
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.

[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.

[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.

Density 1.2±0.1 g/cm3
Boiling Point 656.8±55.0 °C at 760 mmHg
Molecular Formula C33H33FO6
Molecular Weight 544.610
Flash Point 351.0±31.5 °C
Exact Mass 544.226135
PSA 85.22000
LogP 7.61
Vapour Pressure 0.0±2.1 mmHg at 25°C
Index of Refraction 1.594
Storage condition -20°C
Hazard Codes Xi
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