ethambutol

Ethambutol（乙胺丁醇）是可口服的抗结核病药物，也可能够干扰阿拉伯半乳聚糖（arabinogalactan）从而抑制细胞壁合成并抑菌，还可以用于高尿酸血症和视神经病变的动物建模。

Ethambutol dihydrochloride (CL40881) 能抗分枝杆菌，可抑制阿拉伯糖基转移酶活性来阻止细胞壁形成。

Ethambutol.2HCl-d4 是 Ethambutol.2HCl 的氘代化合物。

Ethambutol, (R, R)- can be used to treat tuberculosis. It is usually used in combination with other tuberculosis medications. It may also be used to treat Mycobacterium avium complex, and Mycobacterium kansasii.

Ethambutol-d8 是 Ethambutol 的氘代化合物。Ethambutol 的 CAS 号为 74-55-5。

Ethambutol-KLH 是由 Ethambutol 与 血蓝蛋白 (KLH) 缀合而成的抗原-佐剂偶联物。通过抗原与蛋白佐剂的缀合，能够促进疫苗模型中产生抗原特异性抗体。该缀合物不会影响蛋白质的折叠或损害主要表位，同时可增强交叉呈递和抗原特异性 T 细胞的产生。

Ethambutol-BSA 是一种由 Ethambutol 与 牛血清白蛋白 (BSA) 形成的抗原-佐剂偶联物。该缀合物可以在疫苗模型中提高抗原特异性抗体的生成，而不会干扰蛋白质的折叠或破坏主要表位。此外，它还能促进交叉呈递和抗原特异性 T 细胞的产生。

Dinitrosoethambutol is a biochemical.

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.