quinolone and fluoronaphthyridone ring systems. MAPK inhibitor For this purpose, the (1)H- and (13)C- one- and two-dimensional homo- and heteronuclear NMR methods were used. The analysis of (1)H-

and (13)C-NMR spectra confirmed the structures of investigated fluoroquinolone salts. Relationships between (1)H- and (13)C-NMR chemical shifts of fluoronaphthyridone and fluoroquinolone ring systems, calculated molecular descriptors (MDs) and drug-likeness scores (DLSs), computed for monoprotonic cations of investigated fluoroquinolone salts (TVAH(+), PFXH(+) and C1PH(+)), were also explored. The topological polar surface area (TPSA), the parameter of lipophilicity (miLogP), the relative molecular mass (M(r)) and the volume (V) of computed molecular descriptors (MDs), as well as the G protein-coupled receptor ligand-likeness (GPCR ligand-Is), the ion channel ligand-likeness (ICL-1s), the kinase inhibitor-likeness (K1-1s) and the nuclear receptor ligand-likeness (NRL-1s) were used in this study. The (1)H-NMR chemical shifts of protons in COOH, H5 and NH(n)(+), as well as (13)C-NMR chemical shifts of C4, C5 and C11 shown to be good parameters in exploration of property-property and property-drug-likeness relationships for investigated fluoroquinolone salts. Thus, collinear relationships of (1)H-NMR chemical shifts of protons in COOH, H5 and NH with TPSA and miLogP, as well as with GPCR

ligand-Is, KI-Is and NRL-ls were revealed (delta, ppm H in COOH vs. TPSA, R = -0.9421; delta, ppm H in COOH vs. NRL-ls, R = -0.9216; 8, ppm H5 vs. miLogP, R = 0.9962; delta, ppm H5 vs. KI-Is, R = 0.9969; delta, ppm NH(n)(+) vs. TPSA, R = 0.9875 and 6, ppm NH(n)(+) TGF-beta inhibitor vs. NRL-ls, R = -0.9948). The collinearities between, (13)C-NMR chemical

shifts of C4, C5 and C11 with KI-Is and NRL-ls, as well as with TPSA, miLogP, PXD101 Mr and V were also revealed (delta, ppm C4 vs. TPSA, R = 0.9964; delta, ppm C4 vs. miLogP, R = 0.9487; delta, ppm C4 vs. M(r), R =0.9629; delta, ppm C4 vs. KI-Is, R = 0.9461; delta, ppm C4 vs. NRL-ls, R = 0.9996; delta, ppm C5 vs. miLogP, R = 0.9994; delta, ppm C5 vs. KI-Is, R = 0.9990; delta, ppm C5 vs. NRL-ls, R = 0.9510; delta, ppm Cu vs. TPSA, R = -0,9958; delta, ppm C11 vs. NRL-ls, R = 0.9994 and delta, ppm Cll vs. KT-1s, R = – 0.9481).”
“SETTING: A tertiary care centre in Mumbai, India.

OBJECTIVE: To estimate the extent of association between inhA mutant isoniazid (INH) resistant strains and ethionamide (ETH) resistance.

DESIGN: A total of 140 clinical isolates processed for INH and ETH phenotypic drug susceptibility testing, and molecularly processed with the line-probe assay (LPA) Genotype (R) MTBDRplus, were considered.

RESULTS: Among the 112 phenotypically determined INH-resistant strains, 69 (61.6%) strains were ETH-resistant. An inhA promoter mutation was identified in 24 (21.4%) INH-resistant isolates, 21 (87.5%) of which were ETH-resistant (P < 0.0001).