inh 1

INH1 (IBT13131) 通过直接结合Hec1，特异性干扰 Hec1 Nek2 的相互作用。它在体内外均表现出良好的抗肿瘤活性。

ODN INH-1 是一个回文抑制性寡核苷酸，也是TLR9诱导的B细胞和巨噬细胞的有效抑制剂。

T3Inh-1 是一种有效的选择性 ppGalNAc-T3 抑制剂，IC50 为 7 µM。 T3Inh-1 可预防乳腺癌细胞。 T3Inh-1 降低组织细胞和小鼠中的 FGF23 激素水平，而不会引起任何毒副作用。

Inh2-B1是一种针对STK1（即Ser Thr蛋白激酶）的抑制剂，通过直接结合到STK1的ATP结合催化区域发挥作用。STK1是金黄色葡萄球菌细胞壁生物合成的重要组成部分，且是导致MRSA耐药性的关键因素。因此，Inh2-B1被视为一种“抗生素耐药性破解剂”，具有阻止生物膜形成的功能。

UTA1inh-A1 is a novel inhibitor of kidney urea transporter UT-A1.

UTA1inh-B1 is a novel inhibitor of kidney urea transporter UT-A1.

UTA1inh-C1 is a novel inhibitor of kidney urea transporter UT-A1.

UTA1inh-D1 is a novel inhibitor of kidney urea transporter UT-A1 .

PAT1inh-B01为选择性SLC26A6抑制剂，抑制PAT1（Cl- HCO3-交换器）介导的阴离子交换（IC50: 350 nM），并阻断小肠液体吸收，适用于小肠分泌不足相关疾病研究。

PAT1inh-A0030 是一种选择性 PAT1 (SLC26A6) 抑制剂 (IC50 = 1.0 μM)。在肠道液体吸收闭环模型中，PAT1inh-A0030 抑制野生型和囊性纤维化 (CF) 小鼠 (CftrdelF508 delF508) 回肠的液体吸收，可用于 CF 相关肠道疾病的研究。

CFTR(inh)-172 (CFTR Inhibitor-172) 是一种不依赖电压的选择性 CFTR 抑制剂，在2分钟内可逆地抑制CFTR 短路电流的Ki 值为300 nM。

INH154 是一种高效的 Nek2 和 Hec1 结合抑制剂，能够抑制 Hela 细胞(IC50:200 nM)、 MB468 细胞(IC50:120 nM)。

Ajugamarin H1 是一种天然化合物，可作为天然产物对照品。

Prostaglandin H1 是 DGLA 的环氧化酶代谢物，也是一种 CRTh2 激动剂以及 1 系列抗炎前列腺素的前体物质。Prostaglandin H1 可用于炎症的研究。

INH14 是 IKKα (IC50:8.97 μM) IKKβ (IC50:3.59 μM) 的抑制剂。它能够抑制 IKKα β 依赖性 TLR 炎症反应，抑制 TAK1 TAB1 的下游和 NF-kB 信号通路。它具有抗炎和抗癌作用。

Sanguiin h 11 is a compound purified from the plant Sanguisorba officinalis and has proven to be a potent inhibitor of chemoattractant-dependent and independent neutrophil movement.

MK-8712 is a monobactam beta-lactamase inhibitor.

INH-13 is a Aurora inhibitor.

Maximin H1是一种抗菌肽，由中华红腹蟾蜍(Bombina maxima)皮肤分泌物提取得到。该化合物对Escherichia coli ATCC 25922、Staphylococcus aureus ATCC 25923、Bacillus pyocyaneus CMCC B1010和Candida albicans ATCC 2002表现出抗菌活性，其最小抑菌浓度(MIC)值分别为9、4.5、9、4.5 μg ml。

Bombinin H1是Bombina variegata蛾皮肤中提取的抗菌肽。该肽对大肠杆菌D21的致死浓度为3.8μM，而对金黄色葡萄球菌Cowan 1的致死浓度为2.1μM。

Biotin-H10，作为一种特异性抑制剂，针对前梯度蛋白2 (AGR2)，其KD值为6.4 nM。此化合物能有效抑制癌细胞活力。

RNF5 agonist 1 (analog-1) 是 RNF5 inhibitor inh-02 的结构类似物，也是一种有效的 RNF5 激动剂。在表达 CFBE41o- 的 F508del-CFTR 细胞中，RNF5 agonist 1 能够增加 ATG4B 的泛素化状态。

RNF5 inhibitor inh-02, a potent E3 ubiquitin ligase RNF5 RMA1 inhibitor, demonstrates significant efficacy in rescuing F508del-CFTR with an EC50 of 2.2 uM in bronchial epithelial cells homozygous for the F508del mutation. This compound is valuable for cystic fibrosis research[1].

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.