inh 1

INH1 (IBT13131) is a cell-permeable Hec1 inhibitor that specifically disrupts the Hec1/Nek2 interaction.

T3Inh-1 is an effective and selective inhibitor of ppGalNAc-T3 with an IC50 of 7 µM. T3Inh-1 prevents breast cancer cells. T3Inh-1 reduces FGF23 hormone levels in both tissue cells and mice, without causing any toxic side effects.

PAT1inh-B01, a selective SLC26A6 inhibitor, impedes PAT1 (a Cl-/HCO3- exchanger) activity, with an IC50 of 350 nM, effectively inhibiting anion exchange. It also obstructs fluid absorption in the small intestine and is utilized in the study of small intestinal hyposecretory disorders [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.

ODN 105870, a G-modified inhibitory oligonucleotide (INH-ODN), selectively inhibits TLR7 and is used in the study of inflammatory immune responses [1].

ODN 20844, a guanine-modified inhibitory oligonucleotide (INH-ODN), serves as an inhibitor for TLR7 and TLR9 (Toll-like receptors), originating from its parent compound INH-ODN 2088. It specifically impedes immune cell responses mediated by TLR7 and TLR9. The sequence of ODN 20844 is 5'-TCCTGGCGc7GGGAAGT-3' [1].

ODN 24991, a guanine-modified inhibitory oligonucleotide (INH-ODN) derivative of INH-ODN 2088, inhibits Toll-like receptors (TLR) 3, TLR7, and TLR9, thereby attenuating TLR3-, TLR7-, and TLR9-mediated immune responses. The sequence of ODN 24991 is 5'-C-C-T-G-G-C-c7rGm-G-G-G-3' [1].

ODN 105871, a G-modified inhibitory oligonucleotide (INH-ODN), serves as a selective inhibitor of Toll-like receptor 7 (TLR7) and is used in the study of inflammatory immune responses [1].

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].

ODN 21595, a guanine-modified inhibitor targeting TLR7 and TLR9, effectively inhibits the release of IFN-α and IL-6 without exhibiting cytotoxicity. It also reduces the expression of CD86 and HLA-DR, showcasing potential for systemic lupus erythematosus (SLE) research [1].

Mtb-IN-4 (compound 17h) is a non-toxic isoxazole that exhibits anti-Mycobacterium tuberculosis (Mtb) activity with an IC50 value of 0.70 μM. It impedes Mtb respiration and biofilm formation within macrophages and augments the efficacy of the antibiotic isoniazid (INH) against INH-resistant Mtb mutants [1].

Mtb-IN-5 (compound (-)17j) is an isoxazole with anti-Mycobacterium tuberculosis (Mtb) activity, inhibiting Mtb respiration and biofilm formation within macrophages, and enhancing the efficacy of the antibiotic isoniazid (INH) against INH-resistant Mtb mutants [1].

ODN 24888, a guanine-modified inhibitory oligonucleotide (INH-ODN), effectively inhibits TLR7/TLR9-mediated signaling, reducing IFN-α levels and NF-κB activation, and suppressing IL-6 release. This compound plays a role in modulating immune and inflammatory responses and has potential applications as a vaccine adjuvant [1] [2].

Thiocarlide (isoxyl) is a thiourea derivative that was used in the 1960s to successfully treat tuberculosis (TB). It has considerable antimycobacterial activity in vitro and is effective against multi-drug resistant strains of Mycobacterium tuberculosis in the range of 1-10 µg/ml. [1] [2] At concentrations of 10 µM, isoxyl inhibits the synthesis of M. bovis during six hours of exposure which is similar to isoniazid (INH) and ethionamide (ETH), two other predominant anti-tuberculosis drugs. Unlike INH and ETH, isoxyl also partially inhibits the synthesis of fatty acids. Isoxyl shows no acute toxicity against primary macrophage cell cultures as demonstrated by diminution of redox activity.[2]