h-10

JH-LPH-107, an LpxH inhibitor, exhibits a low spontaneous resistance rate and a high safety margin in vitro.

AGH-107 is a highly selective 5-HT7 receptor agonist that can cross the blood-brain barrier, featuring a Ki value of 6 nM and an EC50 value of 19 nM. Demonstrating high selectivity for central nervous system targets, AGH-107 also exhibits high metabolic stability and low toxicity in HEK-293 and HepG2 cell cultures.

AH-1058 HCl is a lipophilic antiarrhythmic calcium channel blocker.

GlyH-101 is a cell-permeable glycinyl hydrazone compound that blocks CFTR with Ki of 1.4 uM.

AH-1058 free base is a biochemical.

CH-100 is a Chinese herbal medicine previously used in the treatment of human hepatitis C.

UCPH-101 is an inhibitor of excitatory amino acid transporter subtype 1 (EAAT1) with an IC50 of 0.66 μM.

BPH-1086 (compound 10) is an inhibitor of IspH, a domain that, when fused with ribosomal protein S1 (RPS1), can bind to mRNA or form part of the bacterial ribosome [1] [2].

UCPH-102 can be used in Alzheimer's disease, amyotrophic lateral sclerosis, chronic pain and obsessive compulsive disorder studies with good blood-brain permeability. UCPH-102 is a highly selective inhibitor of EAAT1 with an IC50 value of 0.43 μM. UCPH-102 also shows a specific anti-proliferative effect on T-ALL cells [1] [2] [3] [4].

WH-10417-099 is a degrader capable of inducing the degradation of over 125 unique kinases [1].

Oltipraz (RP 35972) is a synthetic dithiolethione with potential chemopreventive and anti-angiogenic properties. Oltipraz induces phase II detoxification enzymes, such as glutathione S transferase (GST) and NAD(P)H: quinone oxidoreductase 1 (NQO1). The induction of detoxification enzymes enhances the detoxification of certain cancer-causing agents, thereby enhancing their elimination and preventing carcinogen-induced DNA damages. Although the exact mechanism through which the anti-angiogenesis effect remains to be fully elucidated, oltipraz maybe able to modulate the expression of a number of angiogenic factors, thereby blocking the sustained and focal neovascularization in multiple tumor cell types.

Beauveriolide III, a cyclodepsipeptide found in Beauveria fungi, inhibits lipid droplet formation (at 3-10 μM) and cholesterol synthesis (IC50=0.41 μM). This compound also suppresses acyl-coenzyme A:cholesterol acyltransferase (ACAT) activity (IC50=5.5 μM) and reduces atherosclerotic lesion size in Ldlr-/- and ApoE-/- mouse models (25-50 mg/kg).

PROTAC PARP1 degrader is a degrader of PARP1 based on the PROTAC technology. PROTAC PARP1 degrader at 10 μM at 24 h inhibits MDA-MB-231 cell line (IC50 of 6.12 μM).

AM679 is a potent and selective FLAP inhibitor with IC50s of 2.2 nM/0.6 nM/154 nM for FLAP binding/hLA/hWB respectively. IC50 value: 2.2 nM/0.6 nM/154 nM(FLAP binding/hLA/hWB) [1] AM679 showed an improved CYP inhibition profile (IC50 3A4 = 16.7 lM, 2C9 =

AZD7687 is a potent and selective DGAT1 inhibitor with an IC50 value of 80 nM (hDGAT1). IC50 value: 80 nM [1] Target: DGAT1 in vitro: Plasma AZD7687 exposure was measured repeatedly. AZD7687 markedly reduced postprandial TAG excursion with a steep concent

CGP60474 is an inhibitor of VEGFR-2 (IC50 = 84 nM) and an inhibitor of ATP-competitive PKC. CGP60474 is also a highly potent anti-endotoxemic agent and inhibits cyclin-dependent kinase (CDK) potently.

FTI-2153 is a potent and highly selective farnesyltransferase (FTase) inhibitor (IC50: 1.4 nM) that is over 3000-fold more effective at blocking H-Ras (IC50: 10 nM) than Rap1A processing.

Cyclosporin H (CsH), a specific inhibitor of FPR1, inhibited lung inflammation in the ALI models. CsH significantly attenuated MTDs or NFP-induced inflammatory lung injury and activation of MAPK and AKT pathways. Cyclosporin H is a viral transduction enha

Fluconazole (hydrate) is a triazole antifungal agent used for oral treatment and prevention of both superficial and systemic fungal infections, including but not limited to balanitis, various Candida infections, Cryptococcus infections, dermatomycosis, and fungal infections of the respiratory and urinary tracts. As the hydrate salt form of fluconazole, it exhibits antifungal activity by inhibiting the growth and development of pathogenic fungi, such as Candida species, at minimal inhibitory concentrations often exceeding 100 mg/l. Notably, it disrupts the branching and hyphal formation in C. albicans at concentrations as low as 0.3 mg/l, indicating its potency compared to other antifungals like miconazole and ketoconazole which are effective at 100-fold lower concentrations. Clinical studies have not shown a significant increase in the risk of most birth defects with oral fluconazole, although there may be an associated risk of tetralogy of Fallot. Its efficacy against Cryptococcus gattii in koalas suggests it may be ineffective as a sole therapeutic agent at a dosage of 10 mg/kg orally every 12 h. Toxicity symptoms from overdose can include hallucinations and paranoid behavior.

KC01 is an effective and selective inhibitor of ABHD16A. By measuring competitive gel-based ABPP (IC50 values of inhibition of ABHD16A by KC01 and KC02: ~0.2–0.5 μM and >10 μM, respectively). Testing by a PS substrate assay, IC50 values of inhibition of h

Msh (5-10), cyclic, as a synthetic peptide, can conjugate with fatty acids for enhanced potency.

NLCQ-1 is a novel weak DNA-intercalative bioreductive compound. NLCQ-1 exhibited a C50 of 44 microM. NLCQ-1 demonstrated significant hypoxic selectivity in several rodent (V79, EMT6, SCCVII) or human (A549, OVCAR-3) tumor cell lines. Its potency as a hypo

β-Rubromycin is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities.1 It inhibits the growth of HMO2, KATO-III, and MCF-7 cells with GI50 values of 0.5, 0.84, and <0.1 μM, respectively. β-rubromycin inhibits HIV-1 reverse transcriptase activity by 39.7% when used at a concentration of 10 μM. It also has antibacterial activity against Gram-positive bacteria. The structure of β-rubromycin was originally described as containing an ortho-quinone group, but it was revised to a para-quinone group in 2000 using organic and biosynthetic methods, as well as spectroscopic analysis.1,2,3References1. Ueno, T., Takahashi, H., Oda, M., et al. Inhibition of human telomerase by rubromycins: Implication of spiroketal system of the compounds as an active moiety. Biochemistry 39(20), 5995-6002 (2000).2. Puder, C., Loya, S., Hizi, A., et al. Structural and biosynthetic investigations of the rubromycins. Eur. J. Org. Chem. 2000(5), 729-735 (2000).3. Goldman, M.E., Salituro, G.S., Bowen, J.A., et al. Inhibition of human immunodeficiency virus-1 reverse transcriptase activity by rubromycins: Competitive interaction at the template.primer site. Mol. Pharmacol. 38(1), 20-25 (1990). β-Rubromycin is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities.1 It inhibits the growth of HMO2, KATO-III, and MCF-7 cells with GI50 values of 0.5, 0.84, and <0.1 μM, respectively. β-rubromycin inhibits HIV-1 reverse transcriptase activity by 39.7% when used at a concentration of 10 μM. It also has antibacterial activity against Gram-positive bacteria. The structure of β-rubromycin was originally described as containing an ortho-quinone group, but it was revised to a para-quinone group in 2000 using organic and biosynthetic methods, as well as spectroscopic analysis.1,2,3 References1. Ueno, T., Takahashi, H., Oda, M., et al. Inhibition of human telomerase by rubromycins: Implication of spiroketal system of the compounds as an active moiety. Biochemistry 39(20), 5995-6002 (2000).2. Puder, C., Loya, S., Hizi, A., et al. Structural and biosynthetic investigations of the rubromycins. Eur. J. Org. Chem. 2000(5), 729-735 (2000).3. Goldman, M.E., Salituro, G.S., Bowen, J.A., et al. Inhibition of human immunodeficiency virus-1 reverse transcriptase activity by rubromycins: Competitive interaction at the template.primer site. Mol. Pharmacol. 38(1), 20-25 (1990).

β-Defensin-2 is a peptide with antimicrobial properties that protects the skin and mucosal membranes of the respiratory, genitourinary, and gastrointestinal tracts.1It inhibits the growth of periodontopathogenic and cariogenic bacteria, includingP. gingivalisandS. salivarius.2β-Defensin-2 (30 μg/ml) stimulates gene expression and production of IL-6, IL-10, CXCL10, CCL2, MIP-3α, and RANTES by keratinocytes.3It also stimulates calcium mobilization, migration, and proliferation of keratinocytes when used at concentrations of 30, 10, and 40 μg/ml, respectively. β-Defensin-2 induces IL-31 production by human peripheral blood-derived mast cellsin vitrowhen used at a concentration of 10 μg/ml and by rat mast cellsin vivofollowing a 500 ng intradermal dose.4Expression of β-defensin-2 is increased in psoriatic skin and chronic wounds.5,6 1.Lehrer, R.I.Primate defensinsNat. Rev. Microbiol.2(9)727-738(2004) 2.Ouhara, K., Komatsuzawa, H., Yamada, S., et al.Susceptibilities of periodontopathogenic and cariogenic bacteria to antibacterial peptides, β-defensins and LL37, produced by human epithelial cellsJ. Antimicrob. Chemother.55(6)888-896(2005) 3.Niyonsaba, F., Ushio, H., Nakano, N., et al.Antimicrobial peptides human β-defensins stimulate epidermal keratinocyte migration, proliferation and production of proinflammatory cytokines and chemokinesJ. Invest. Dermatol.127(3)594-604(2007) 4.Niyonsaba, F., Ushio, H., Hara, M., et al.Antimicrobial peptides human β-defensins and cathelicidin LL-37 induce the secretion of a pruritogenic cytokine IL-31 by human mast cellsJ. Immunol.184(7)3526-3534(2010) 5.Huh, W.-K., Oono, T., Shirafuji, Y., et al.Dynamic alteration of human β-defensin 2 localization from cytoplasm to intercellular space in psoriatic skinJ. Mol. Med. (Berl.)80(10)678-684(2002) 6.Butmarc, J., Yufit, T., Carson, P., et al.Human β-defensin-2 expression is increased in chronic woundsWound Repair Regen.12(4)439-443(2004)