BMS-186318 - CAS 161302-40-5
Catalog number: 161302-40-5
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C36H54N4O9
Molecular Weight:
686.85
COA:
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Targets:
HIV Protease
Description:
BMS-186318 has been found to be a HIV protease inhibitor that was once studied against HIV by Bristol-Myers Squibb.
Purity:
98%
Appearance:
Powder
Synonyms:
BMS 186318; BMS-186318; BMS186318; 12-Oxa-2,6,10-triazatetradecanoic acid, 4,8-dihydroxy-13,13-dimethyl-3-((4-(2-(4-morpholinyl)-2-oxoethoxy)phenyl)methyl)-11-oxo-9-(phenylmethyl)-, 1,1-dimethylethyl ester, (3S,4R,8R,9S)-; BMS-186318 analog 19; 12-Oxa-2,6,10-triazat
Storage:
Store in a cool and dry place and at 0 - 4 °C for short term (days to weeks) or -20 °C for long term (months to years).
MSDS:
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Quality Standard:
In-house standard
Quantity:
Milligram-Grams
InChIKey:
OQHZMGOXOOOFEE-SYQUUIDJSA-N
InChI:
InChI=1S/C36H54N4O9/c1-35(2,3)48-33(44)38-28(20-25-10-8-7-9-11-25)30(41)22-37-23-31(42)29(39-34(45)49-36(4,5)6)21-26-12-14-27(15-13-26)47-24-32(43)40-16-18-46-19-17-40/h7-15,28-31,37,41-42H,16-24H2,1-6H3,(H,38,44)(H,39,45)/t28-,29-,30+,31+/m0/s1
Canonical SMILES:
CC(C)(C)OC(=O)NC(CC1=CC=CC=C1)C(CNCC(C(CC2=CC=C(C=C2)OCC(=O)N3CCOCC3)NC(=O)OC(C)(C)C)O)O
1.Determination of BMS-186318 in dog, rat and monkey plasma by liquid chromatography-ionspray mass spectrometry.
Jemal M;Hawthorne D J Pharm Biomed Anal. 1995 Dec;14(1-2):43-8.
BMS-186318 is a member of the recently discovered "aminodiol" class of HIV protease inhibitors. A simple but sensitive method was developed for the determination of BMS-186318 in dog plasma and then applied to monkey and rat plasma. The compound was extracted from dog plasma with methyl tert-butyl ether at basic pH. The dried extract was reconstituted in mobile phase and injected into a 150 x 2.1 mm i.d. Zorbax Rx-C18 HPLC column. A portion of the effluent was directed into the LC-ionspray MS system, where the [M+H]+ ion of the secondary amine compound was monitored. The HPLC conditions were chosen in order to achieve a short run time and large sample throughput, with both analyte and internal standard eluting within 1.5 min. The liquid-liquid extraction procedure provided very clean extracts so that sufficient signal-to-noise ratio was obtained with single-stage mass spectrometry instead of the more costly tandem mass spectrometry. The required lower limit of quantitation of 2.5 ng ml-1 was easily achieved. The method has also been validated for BMS-186318 in monkey plasma without modification. The method has been modified for rat plasma. Owing to irreproducibility observed when applying the liquid-liquid extraction method to rat plasma, a solid-phase extraction method was developed.
2.Characterization of a human immunodeficiency virus type 1 variant with reduced sensitivity to an aminodiol protease inhibitor.
Patick AK;Rose R;Greytok J;Bechtold CM;Hermsmeier MA;Chen PT;Barrish JC;Zahler R;Colonno RJ;Lin PF J Virol. 1995 Apr;69(4):2148-52.
Development of viral resistance to the aminodiol human immunodeficiency virus (HIV) protease inhibitor BMS 186,318 was studied by serial passage of HIV type 1 RF in MT-2 cells in the presence of increasing concentrations of compound. After 11 passages, an HIV variant that showed a 15-fold increase in 50% effective dose emerged. This HIV variant displays low-level cross-resistance to the C2 symmetric inhibitor A-77003 but remains sensitive to the protease inhibitors Ro 31-8959 and SC52151. Genetic analysis of the protease gene from a drug-resistant variant revealed an Ala-to-Thr change at amino acid residue 71 (A71T) and a Val-to-Ala change at residue 82 (V82A). To determine the effects of these mutations on protease and virus drug susceptibility, recombinant protease and proviral HIV type 1 clones containing the single mutations A71T and V82A or double mutation A71T/V82A were constructed. Subsequent drug sensitivity assays on the mutant proteases and viruses indicated that the V82A substitution was responsible for most of the resistance observed. Further genotypic analysis of the protease genes from earlier passages of virus indicated that the A71T mutation emerged prior to the V82A change.
3.Human immunodeficiency virus type 1 viral background plays a major role in development of resistance to protease inhibitors.
Rose RE;Gong YF;Greytok JA;Bechtold CM;Terry BJ;Robinson BS;Alam M;Colonno RJ;Lin PF Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1648-53.
The observed in vitro and in vivo benefit of combination treatment with anti-human immunodeficiency virus (HIV) agents prompted us to examine the potential of resistance development when two protease inhibitors are used concurrently. Recombinant HIV-1 (NL4-3) proteases containing combined resistance mutations associated with BMS-186318 and A-77003 (or saquinavir) were either inactive or had impaired enzyme activity. Subsequent construction of HIV-1 (NL4-3) proviral clones containing the same mutations yielded viruses that were severely impaired in growth or nonviable, confirming that combination therapy may be advantageous. However, passage of BMS-186318-resistant HIV-1 (RF) in the presence of either saquinavir or SC52151, which represented sequential drug treatment, produced viable viruses resistant to both BMS-186318 and the second compound. The predominant breakthrough virus contained the G48V/A71T/V82A protease mutations. The clone-purified RF (G48V/A71T/V82A) virus, unlike the corresponding defective NL4-3 triple mutant, grew well and displayed cross-resistance to four distinct protease inhibitors. Chimeric virus and in vitro mutagenesis studies indicated that the RF-specific protease sequence, specifically the Ile at residue 10, enabled the NL4-3 strain with the triple mutant to grow.
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