h37rv

BM635 hydrochloride is an MmpL3 inhibitor with outstanding anti-mycobacterial activity (MIC50: 0.12 μM against M. tuberculosis H37Rv).

BM635 mesylate is an MmpL3 inhibitor with outstanding anti-mycobacterial activity (MIC50: 0.12 μM against M. tuberculosis H37Rv).

n-acetylciprofloxacin (3-Quinolinecarboxylic acid, 7-(4-acetyl-1-piperazinyl)-1-cyclopropyl-6-fluoro-1) 是 H37Rv 的抑制剂。

sCNH240(2-Fluoro-N-[3-(3-thienyl)-5-isoxazolyl]benzenesulfonamide)是一种潜在的选择性 Rv1625c Cya 激活剂，具有良好的细胞渗透性和口服活性，在胆固醇补充的7H12培养基中对结核分枝杆菌（Mtb）H37Rv 株的IC90=1.24 µM，对 CYP2C19，CYP2C9 和hERG 通道具有抑制作用。

anti-TB agent 1是一种有效的口服活性抗结核化合物，对结核分枝杆菌H37Rv、rRMP 和rINH 的MICs＜2nM。

Urease Inhibitor 07 是一种异取代金属蛋白酶抑制剂 ， 对结核分枝杆菌H37Rv 菌株的潜在活性。

Thiacetazone (Diazam) 是一种氨基硫脲抗结核剂，也是一种具有口服活性抗生素。它具有抗菌作用，可抑制结核分枝杆菌 H37Rv 的生长，MIC 值为 0.1 μg mL。

TBA-354 有抗结核作用，对结核分枝杆菌 H37Rv 菌株具有活性。

QST4 具有抗结核、抗真菌活性，在结核分枝杆菌 Mycobacterium tuberculosis H37Rv 中的 MIC 值为 6.25 μM。

BM635 is an MmpL3 inhibitor with outstanding anti-mycobacterial activity (MIC50: 0.12 μM against M. tuberculosis H37Rv).

MDRTB-IN-1 (5aα) is an antibiotic which is against Mycobacterium tuberculosis H37Rv(MIC90 :10.5 μM).

NITD-349 是MmpL3的抑制剂，它对毒性结核分枝杆菌 H37Rv 显示出高效的抗分枝杆菌活性，MIC50 为 23 nM。

Mtb-IN-8（compound 5jb）是一种针对结核分枝杆菌（Mtb）的口服活性抑制剂，其对H37Rv的MIC值为0.03 μg mL，而对MDR-Mtb的MIC值介于0.125-0.06 μg mL之间。

VEGFR-2 InhA-IN-1是一种含吡唑结构的双功能抑制剂，既具有抗结核活性也有抗血管生成的效用。该化合物对结核分枝杆菌H37Rv株展示出有效的抑菌作用（MIC=6.25 μg mL），同时对VEGFR-2的抑制也相当显著（IC50=15.27 nM）。

ATP synthase inhibitor3（compound PT6）作为一种分枝杆菌F-ATP合酶抑制剂（IC50=0.788 μM），显示出口服活性。此化合物能有效抑制体外Mycobacterium tuberculosis H37Rv菌株（ATCC-27294）的生长，并在IC50值达30 μM时显著降低细胞内ATP水平。

InhA-IN-8 (compound 6c) 为一种抗结核分枝杆菌InhA（烯酰ACP还原酶）的口服有效抑制剂。此化合物对Mtb UalRv显示出较高的抑制效果（MIC = 0.5-1 μg mL）。InhA-IN-8 同时也适用于进行急性结核模型小鼠的实验研究。

DprE1-IN-11 (compound 3) 作为一种口服活性DprE1抑制剂，针对 MTB H37Rv 和 MDR-MTB 菌株显示出有效的抗结核活性，其最小抑菌浓度 (MIC) 范围为 <0.029-0.095 μM。

HT1171 是一种高效且具选择性的结核分枝杆菌蛋白酶体抑制剂。对结核分枝杆菌 H37Rv 具有显著的抗结核活性，MIC90为 2 μg mL，MIC为 4 μg mL。浓度为 100 μM 时，对人正常肝细胞 L02 的抑制率为 53.8%。HT1171 可用于抗结核药物研究。

Pks13-IN-1 (Compound 44) 是一种口服有效的 Mycobacterium tuberculosis 聚酮合酶 13 (Pks13) 抑制剂。它对结核分枝杆菌 H37Rv 菌株的抑制浓度 (MIC) 为 0.07 μM。在小鼠模型中，Pks13-IN-1 展示了抗菌活性。

Pks13-IN-2 (Compound 43) 是一种口服活性Pks13抑制剂，对结核分枝杆菌 H37Rv 的MIC为 0.8-1.8 μM，显示抑制活性。在小鼠肝微粒体和肝细胞中，Pks13-IN-2 表现出良好的代谢稳定性。它可用于结核病研究。

SB-790594-A is a non-cytotoxic Mycobacterium tuberculosis H37Rv inhibitor.

GSK1829820A is a Mycobacterium tuberculosis H37Rv non-cytotoxic inhibitor.

BTZ043 是一种 DprE1 的抑制剂，它对结核分枝杆菌 H37Rv 和耻垢分枝杆菌具有纳摩尔杀菌活性，MIC 值分别为 2.3 nM 和 9.2 nM。

OPC-167832 is a potent and orally active dprE1 Inhibitor with an IC50 of 0.258 μM. OPC-167832 has antituberculosis activity and can be used for the research of tuberculosis caused by Mycobacterium tuberculosis[1]. OPC-167832 exhibits very low MICs against laboratory strains of M. tuberculosis H37Rv (MIC: 0.0005 μg ml) and Kurono (MIC: 0.0005 μg ml) and strains with monoresistance to rifampin (RIF), isoniazid (INH), ethambutol (EMB), streptomycin (STR), and pyrazinamide (PZA) (MIC: 0.00024-0.001 μg ml). However, OPC-167832 has minimal or no activity against standard strains of nonmycobacterial aerobic and anaerobic bacteria[1].The IC90 values of OPC-167832 against intracellular M. tuberculosis strains H37Rv and Kurono are 0.0048 and 0.0027 μg ml, respectively. OPC-167832 shows bactericidal activity against intracellular M. tuberculosis at a low concentration, and the bactericidal activity is saturated at concentrations of 0.004 μg ml or higher[1]. OPC-167832 (oral administration; 0.625-10 mg kg) exhibits a good pharmacokinetic characteristic. The plasma reaches peak at 0.5 h to 1.0 h (tmax) and is eliminated with a half-life (t1 2) of 1.3 h to 2.1 h OPC-167832 distribution in the lungs is approximately 2 times higher than that in plasma, and the Cmax and AUCt of OPC-167832 in plasma and the lungs shows dose dependency[1].OPC-167832 (oral administration; 0.625-10 mg kg; 4 weeks) significantly reduces lung CFU compared to the vehicle group. The dose-dependent decrease of lung CFU is observed from 0.625 mg kg to 2.5 mg kg. In a M. tuberculosis Kurono-infected ICR female mice model. OPC-167832 combines with DMD, BDQ, or LVX via oral gavage exhibits significantly higher efficacies than each single agent alone[1].[1].OPC-167832 (oral gavage; 2.5 mg kg; combination with DCMB; 12 weeks) demonstrates the most potent efficacy when compares with DC, DCB. The lung CFU count after 6 weeks of treatment is below the detection limit, and at the end of just 8 weeks of treatment, the bacteria in the lungs of all the evaluated mice had already been eradicate[1]. [1]. Norimitsu Hariguchi, et al. OPC-167832, a Novel Carbostyril Derivative with Potent Antituberculosis Activity as a DprE1 Inhibitor.Antimicrob Agents Chemother. 2020 May 21;64(6):e02020-19.