at 121

AT-121 is a dual μ-opioid and neuropeptide receptor partial agonist (Kis 16.49 and 3.67 nM, respectively). It stimulates [35S]GTPγS binding to cell membranes expressing either μ-opioid receptors or neuropeptide receptors (EC50s of 19.6 and 34.7 nM, respectively.) AT-121 (0.003-0.03 mg kg) reduced capsaicin-induced thermal anisocoria in a dose-dependent manner, but did not increase scratching activity in rhesus monkeys. In rhesus monkey drug self-administration tests, AT-121 at doses of 0.3 to 10 μg kg per injection lacked reinforcing effects (a potential marker of abuse) and did not reduce the reinforcing effects of food pellets.AT-121 (0.01 or 0.03 mg kg) did not induce hyperalgesia, a marker of tolerance, in rhesus monkeys.AT-121 is a safe non-addictive pain reliever with anti-injury and analgesic effects.

AT-121 hydrochloride is a dual agonist of nociception and mu opioid receptor with Ki values of 3.67 and 16.49 nM, respectively.AT-121 hydrochloride is a safe, non-addictive, pain relieving compound with anti-injury and analgesic activity. AT-121 hydrochloride is a safe, non-addictive, pain relieving compound with anti-injury and analgesic activity.

CMS-121, a quinolone derivative, is an orally active acetyl-CoA carboxylase 1 (ACC1) inhibitor. CMS-121 protects HT22 cells against ischemia and oxidative damage (EC50: 7 nM and 200 nM). CMS-121 shows strong neuroprotective, antioxidative, anti-inflammatory, and renoprotective activities.

BCI-121 is a substrate-competitive SMYD3 inhibitor that inhibits the proliferation of the cancer cell.

Anticancer agent 121, a human lactate dehydrogenase A (hLDHA) inhibitor, exhibits potent anticancer activities, suitable for use in anticancer research [1].

NS2 (114-121), Influenza, is a fragment derived from the nonstructural protein 2 (NS2) of the influenza virus, serving as an epitope for influenza research and useful for studying CD8+ cytotoxic T lymphocyte (CTL) responses in antiviral immunity.

Reversin 121, a P-glycoprotein inhibitor, enhances MDR1's ATPase activity and counteracts P-glycoprotein-mediated multidrug resistance, making it useful in cancer research.

Antibacterial agent 121 (Compound 10) exhibits antibacterial properties against mycobacterial strains and possesses anti-inflammatory activity, making it a promising candidate for Tuberculosis (TB) research [1].

PP-121 is a multi-targeted inhibitor of PDGFR (IC50: 2 nM), Hck (IC50: 8 nM), mTOR (IC50: 10 nM), VEGFR2(IC50: 12 nM), Src (IC50: 14 nM) and Abl (IC50: 18 nM) , also inhibits DNA-PK (IC50: 60 nM).

MAGL-IN-4 (His121 ARG57) is one of the monoacylglycerol lipase (MAGL) inhibitors in central nervous system-related diseases.

GSK121 is an inhibitor of selective PAD4.

RC 121 is a highly potent somatostatin (SRIF) analog.

A 121 is a non-polyene antifungal antibiotic. It is active against a number of filamentous fungi including some plant and human pathogens.

CYP121A1-IN-1 is a potent inhibitor of CYP121A1, demonstrating favorable activity against Mycobacterium tuberculosis (H37Rv MIC 90 ~6.25 μM, ~2.2 μg mL). It significantly reduces mycocyclosin production by blocking the CYP121A1-mediated conversion of cyclo(l-tyrosyl-l-tyrosyl) to mycocyclosin [1].

YS121 is a dual inhibitor of microsomal prostaglandin E2 synthase-1 (mPGES-1; IC50=3.4 μM) and 5-lipoxygenase (5-LOX; IC50=6.5 μM). YS121 dose-dependently reduces the production of PGE2 with EC50=12 μM in IL-1β-stimulated A549 cells [1].

Sul-121 has anti-oxidative capacity. In experimental chronic obstructive pulmonary disease (COPD) models, Sul-121 HCl inhibits airway inflammation and hyperresponsiveness (AHR) prospectively through inhibition of oxidative stress.

SKA-121 is a selective KCa3.1 activator (EC50s: 109 nM and 4.4 μM for KCa3.1 and KCa2.3, respectively).

TX2-121-1 targets HER3 for proteasome-mediated degradation to inhibit HER3-dependent signalling and growth.

KUS121 is a valosin-containing protein (VCP) modulator that inhibits VCP ATPase activity (IC50= 330 nM).1It inhibits cell death, ATP depletion, and upregulation of C/EBP-homologous protein (CHOP) induced by tunicamycin, an inducer of ER stress, in HeLa cells when used at concentrations of 20, 50, and 50 μM, respectively. KUS121 (100 μM) inhibits ATP depletion and cell death induced by oxygen-glucose deprivation (OGD) in rat primary cortical neurons in anin vitromodel of cerebral ischemia.2It reduces infarction volume and increases the latency to fall in an accelerating rotarod test in a mouse model of focal cerebral ischemia induced by transient distal middle cerebral artery occlusion (MCAO) when administered at a dose of 100 mg/kg immediately following occlusion and again at 50 mg/kg following reperfusion. KUS121 (50 mg/kg) inhibits thinning of the retinal outer nuclear layer and preserves visual function in an rd10 mouse model of retinitis pigmentosa.1 1.Ikeda, H.O., Sasaoka, N., Koike, M., et al.Novel VCP modulators mitigate major pathologies of rd10, a mouse model of retinitis pigmentosaSci. Rep.45970(2014) 2.Kinoshita, H., Maki, T., Yasuda, K., et al.KUS121, a valosin-containing protein modulator, attenuates ischemic stroke via preventing ATP depletionSci. Rep.9(1)11519(2019)

CM121 is a reversible inhibitor of ALDH1A2 that acts specifically on the active site, exhibiting an IC50 of 0.54 μM and a Kd of 1.1 μM. It exerts its inhibitory effect through multiple hydrophobic interactions.

AMK is an active metabolite of the neurohormone melatonin .1,2,3,4It is formed from melatoninviathe metabolic intermediate AFMK that is then deformylated by catalase or formamidase.5,6AMK scavenges singlet oxygenin vitrowhen used at a concentration of 200 μM.1It inhibits the epinephrine- and arachidonic acid-induced production of prostaglandin E2and PGD2in ovine seminal vesicle microsomes in a concentration- and time-dependent manner, as well as LPS-induced increases in COX-2 levels in RAW 264.7 macrophages when used at a concentration of 500 μM.2,3AMK (20 mg/kg) decreases MPTP-induced increases in lipid peroxidation in the cytosol and mitochondria from substantia nigra and striatum in a mouse model of MPTP-induced Parkinson’s disease.4 1.Schaefer, M., and Hardeland, R.The melatonin metabolite N1-acetyl-5-methoxykynuramine is a potent singlet oxygen scavengerJ. Pineal Res.46(1)49-52(2009) 2.Kelly, R.W., Amato, F., and Seamark, R.F.N-acetyl-5-methoxy kynurenamine, a brain metabolite of melatonin, is a potent inhibitor of prostaglandin biosynthesisBiochem. Biophys. Res. Commun.121(1)372-379(1984) 3.Mayo, J.C., Sainz, R.M., Tan, D.-X., et al.Anti-inflammatory actions of melatonin and its metabolites, N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK) and N1-acetyl-5-methoxykynuramine (AMK), in macrophagesJ. Neuroimmunol.165(1-2)139-149(2005) 4.Tapias, V., Escames, G., López, L.C., et al.Melatonin and its brain metabolite N1-acetyl-5-methoxykynuramine prevent mitochondrial nitric oxide synthase induction in parkinsonian miceJ. Neurosci. Res.87(13)3002-3010(2009) 5.Tan, D.-X., Manchester, L.C., Reiter, R.J., et al.Melatonin directly scavenges hydrogen peroxide: A potentially new metabolic pathway of melatonin biotransformationFree Radic. Biol. Med.29(11)1177-1185(2000) 6.Hirata, F., Hayaishi, O., Tokuyama, T., et al.In vitro and in vivo formation of two new metabolites of melatoninJ. Biol. Chem.249(4)1311-1313(1974)

Tpl2 kinase inhibitor is an inhibitor of tumor progression locus 2 (Tpl2; IC50= 0.05 μM).1It is selective for Tpl2 over MEK, p38 MAPK, Src, MK2, and PKC (IC50s = >40, 180, >400, 110, and >400 μM, respectively). Tpl2 kinase inhibitor inhibits LPS-induced TNF-α production in isolated human monocytes and whole blood (IC50s = 0.7 and 8.5 μM, respectively). It enhances differentiation induced by calcitriol in HL-60 and U937 leukemia cells when used at a concentration of 5 μM.2Tpl2 kinase inhibitor (5 μM) inhibits the proliferation of KG-1a leukemia cells.3 1.Garvin, L.K., Green, N., Hu, Y., et al.Inhibition of Tpl2 kinase and TNF-α production with 1,7-naphthyridine-3-carbonitriles: Synthesis and structure-activity relationshipsBioor. Med. Chem. Lett.15(23)5288-5292(2005) 2.Wang, X., and Studzinski, G.P.Expression of MAP3 kinase COT1 is up-regulated by 1,25-dihydroxyvitamin D3 in parallel with activated c-jun during differentiation of human myeloid leukemia cellsJ. Steroid. Biochem. Mol. Biol.121(1-2)395-398(2010) 3.Wang, X., Gocek, E., Novik, V., et al.Inhibition of Cot1/Tlp2 oncogene in AML cells reduces ERK5 activation and up-regulates p27Kip1 concomitant with enhancement of differentiation and cell cycle arrest induced by silibinin and 1,25-dihydroxyvitamin D3Cell Cycle9(22)4542-4551(2010)