dcb.

L594881, also known as 3',4'-Dichlorobenzamil or DCB, is an inhibitor of Na+ Ca2+ exchanger, Na+ transport and sarcoplasmic reticulum Ca2+ release channels. L594881 can inhibit Na+ Ca2+ exchanger, Na+ transport and sarcoplasmic reticulum Ca2+ release channels.

DCB (3,3'-dichlorobenzaldazine) 是 mGluR5 的变构配体，显示出 3,3'-二甲氧基苯扎嗪 (DMeOB) 的负调节作用。 DCB 在 3,3'-二氟苯扎嗪 (DFB) 的帮助下阻断 mGluR 的正变构调节。

Z-Asp-CH2-DCB 是广谱半胱天冬酶的不可逆抑制剂。

Tylophorine analog DCB-3503 is a potential anticancer and immunosuppressive agent. DCB-3503 suppresses the translation of cellular regulatory proteins, including cyclin D1, at the elongation step. DCB-3503 allosterically regulates the ATPase and chaperone activities of HSC70 by promoting ATP hydrolysis in the presence of specific RNA binding motifs (AUUUA) of cyclin D1 mRNA.

Tylophorine, (-)- is a biomedical.

dCBP-1 是基于Cereblon 配体的p300 CBP 的选择性双功能降解剂。dCBP-1可以有效的杀死多发性骨髓瘤细胞，并降低驱动 MYC 表达的致癌增强子活性。

DCBA 是驱虫剂 N-N-diethyl-meta-toluamide (DEET) 的代谢物。尿液中 DCBA 的浓度是评估 DEET 暴露程度的指标。

DCBCI0901 is an inhibitor of phosphatidylinositide 3-kinase (PI3K), raptor-mTOR (mTOR complex 1 or mTORC1) and rictor-mTOR (mTOR complex 2 or mTORC2) with potential antineoplastic activity.

m-Chloro-DCBA is a bioactive chemical.

m-Fluoro-DCBA is a bioactive chemical

DC-BPi-11为溴域PHD转录因子(BPTF)抑制剂，其IC50值为698 nM，对白血病细胞增殖展现出显著的抑制效果。

DC-BPi-03 是一种新型 BPTF-BRD 抑制剂（IC50 为 698.3 nM），具有潜在的抗癌户型，可用于研究白血病。

5’-O-DMTr-2’,2’-difluoro-dC(Bz)-methyl phosphonamidite 是一种广泛具有抗肿瘤活性的嘌呤核苷类似物，主要用于靶向惰性淋巴系统恶性肿瘤。其抗癌机制主要通过抑制 DNA 合成和诱导细胞凋亡 (apoptosis) 来实现。

Rev dC(Bz)-5'-amidite 是一种具有广泛抗肿瘤活性的嘌呤核苷类似物，主要针对惰性淋巴系统恶性肿瘤。其抗癌机制包括抑制 DNA 合成和诱导细胞凋亡(apoptosis)等作用。

DMT-5Me-dC(Bz)-CE Phosphoramidite 用于生产锁定核酸（LNAs），旨在优化荧光寡核苷酸探针的设计，从而提升其光谱性质和对目标的结合能力。

DC-BPi-11 hydrochloride是一种作用于溴域PHD转录因子(BPTF)的抑制剂，具有698 nM的IC50值。它对白血病细胞的增殖表现出显著的抑制效果。

Nucleoside Derivatives - Fluoro-modified nucleosides; 2'-Modified nucleosides; Nucleoside Phosphoramidites

3'-dC(Bz)-2'-phosphoramidite is a Nucleoside Phosphoramidite.

Nucleoside phosphonamidite;Fluoro-modified nucleosides;2'-Modified nucleosides

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.