Bindarit(AF-2838), a CCL2, CCL7 and CCL8 inhibitor, is an anti-inflammatory agent.Target: OthersBindarit exhibits selective inhibition against monocyte chemotactic proteins MCP-1/CCL2, MCP-3/CCL7 and MCP-2/CCL8. Oral administration of Bindarit at 50 mg/kg in NZB/W mice delays the onset of proteinuria, significantly protects from renal function impairment, and prolongs survival of NZB/W mice or lupus mice. Bindarit treatment completely MCP-1 up-regulation during the progression of nephritis [1]. Inhibition of MCP-1 with Bindarit also reduces tumor growth and macrophage recruitment, rendering necrotic tumor masses in human melanoma xenografts [2]. Bindarit is effective in reducing neointima formation in both non-hyperlipidaemic and hyperlipidaemic animal models of vascular injury by a direct effect on VSMC proliferation and migration and by reducing neointimal macrophage content [3]. Administration of Bindarit results in impaired metastatic disease in prostate cancer PC-3M-Luc2 xenograft mice and impairment of local tumorigenesis in Balb/c mice with murine breast cancer 4T1-Luc cells. In addition, Bindarit treatment significantly decreases the infiltration of tumor-associated macrophages and myeloid-derived suppressor cells in 4T1-Luc primary tumors [4].
SPDB-DM4 is a drug-linker conjugate for ADC by using the maytansinebased payload (DM4) via a SPDB linker, exhibiting potent anti-tumor activity.
19:0 Lyso PG-d5 is deuterium labeled 19:0 Lyso PG.
cGAMP(Cyclic GMP-AMP) is an endogenous second messenger in metazoans and triggers interferon production in response to cytosolic DNA; STING ligand.Target:in vitro: cGAMP induced IFNβ RNA robustly even at concentrations as low as 10 nM. cGAMP was much more potent than c-di-GMP in inducing IFNβ based on ELISA assays. cGAMP was also more potent than c-di-GMP and c-di-AMP in activating IRF3. cGAMP binds to and activates STING to trigger the downstream signaling cascades [1]. On stimulation with cGAMP, fibroblasts from the patients showed increased transcription of IFNB1 but not of the genes encoding interleukin-1 (IL1), interleukin-6 (IL6), or tumor necrosis factor (TNF) [3]. cGAMP activates the endoplasmic reticulum (ER)-resident receptor STING, thereby inducing an antiviral state and the secretion of type I IFNs [4].in vivo: cGAMP can enhance the adaptive immune response to the model antigen ovalbumin in mice. cGAMP promotes antigen specific IgG and a balanced Th1/Th2 lymphocyte response in immunized mice [2].
Thymidine-13C5,15N is the 13C and 15N labeled Thymidine. Thymidine, a specific precursor of deoxyribonucleic acid, is used as a cell synchronizing agent. Thymidine is a DNA synthesis inhibitor that can arrest cell at G1/S boundary, prior to DNA replicatio
Halofantrine hydrochloride (SKF-102886) is a blocker of delayed rectifier potassium current via the inhibition of human-ether-a-go-go-related gene (HERG) channel and a potent antimalarial compound[1][2].
Azido-PEG4-NHS-ester is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs[1].
Danicopan, a selective and orally active small-molecule factor D inhibitor, inhibits alternative pathway of complement (APC) activity. Danicopan has potential to block the alternative pathway of complement in paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS)[1].
Medetomidine(Domtor) is a potent, highly selective α2-adrenoceptor agonist (Ki values are 1.08 and 1750 nM for α2- and α1-adrenoceptors respectively). IC50 value:Target: α2-adrenoceptorMedetomidine displays greater selectivity over α1-adrenoceptors than clonidine and UK 14,304 (1620-, 220- and 300-fold respectively). Medetomidine inhibits twitch response in electrically stimulated mouse vas deferens (pD2 = 9.0). Active in vivo; displays hypotensive, bradycardic, sedative, anxiolytic, hypothermic and analgesic effects.
H-Glu-OtBu.HCl is a glutamic acid derivative[1].
1-Oleoyl-2-acetyl-sn glycerol is a synthetic, cell permeable diacylglycerol analog. 1-Oleoyl-2-acetyl-sn glycerol activates calcium-dependent protein kinase C (PKC) and induces the superoxide-production.
Mifamurtide sodium (MTP-PE sodium), an analog of the muramyl dipeptide (MDP), is a nonspecific immunomodulator by stimulating the immune response activating macrophages and monocytes. Mifamurtide sodium, an orphan drug, is a specific ligand of NOD2 used as an insulin sensitizer. Mifamurtide sodium has the potential for osteosarcoma research[1][2][3].
N-(5-Amino-1-ribosyl-4-imidazolecarbonyl)-L-aspartic acid is a nucleoside metabolite[1].
(2S,3S)-H-Abu(3-N3)-OH (hydrochloride) is a click chemistry reagent containing an azide group[1].
Puromycin aminonucleoside is the aminonucleoside portion of the antibiotic puromycin, and a puromycin analog which does not inhibit protein synthesis or induce apoptosis.
BIIB091 is a highly selective, reversible BTK inhibitor for treating autoimmune diseases.
c-Met-IN-12 (compound 4r) is an orally active, potent and selective type II c-Met kinase inhibitor, with an IC50 of 10.6 nM. c-Met-IN-12 displays high inhibitory effects (inhibition rate > 80% in 1 μM) against AXL, Mer and TYRO3 kinases. c-Met-IN-12 can be used a scaffold for further kinase selectivity enhancement. c-Met-IN-12 shows antitumor efficacy[1].
4-Isopropylbenzyl alcohol is a chemical composition of the essential oils from the leaves and flowers of Camellia nitidissima. C. nitidissima possess multiple biological activities including antioxidant activity, anticancer activity, and cytotoxicity as well as inhibiting the formation of advanced glycation end-products[1].
Morinidazole R enantiomer is the R-enantiomer of Morinidazole. Morinidazole is a new 5-nitroimidazole class antimicrobial agent. Morinidazole R enantiomer is the less active enantiomer.
TL02-59 is an orally active, selective Src-family kinase Fgr inhibitor with an IC50 of 0.03 nM. TL02-59 also inhibits Lyn and Hck with IC50s of 0.1 nM and 160 nM, respectively. TL02-59 potently suppresses acute myelogenous leukemia (AML) cell growth[1].
S0859, an N-cyanosulphonamide compound, reversibly inhibit NBC-mediated pH(i) recovery (K (i)=1.7 microM, full inhibition at approximately 30 microM). IC50 value:Target: NBCNa(+)-coupled HCO(3)(-) transporters (NBCs) mediate the transport of bicarbonate ions across cell membranes and are thus ubiquitous regulators of intracellular pH. NBC dysregulation is associated with a range of diseases; for instance, NBCn1 is strongly up-regulated in a model of ErbB2-dependent breast cancer, a malignant and widespread cancer with no targeted treatment options, and single-nucleotide polymorphisms in NBCn1 genetically link to breast cancer development and hypertension. Treatment with NBC inhibitor S0859 significantly increased caspase-3 activity and elevated the number of apoptotic EC. S0859 is potentially important for probing the transporter's functional role in heart and other tissues.
N1-methyl-pseudouridine (1-Methylpseudouridine), a methylpseudouridine, outperforms 5 mC and 5 mC/N1-methyl-pseudouridine in translation. N1-methyl-pseudouridine in mRNA enhances translation through eIF2α-dependent and independent mechanisms by increasing ribosome density[1].
MDL-811, an allosteric SIRT6 activator, significantly activates SIRT6 histone H3 deacetylation (H3K9Ac, H3K18Ac, and H3K56Ac). MDL-811 could be used in the study of colorectal cancer[1].
N-(((9H-Fluoren-9-yl)methoxy)carbonyl)-S-methyl-L-cysteine is a cysteine derivative[1].
Penetratin is a peptide derived from the amphiphilic Drosophila Antennapedia homeodomain[1].
Ms-PEG2-Ms is a PEG-based PROTAC linker that can be used in the synthesis of PROTACs[1].
Nurr1 agonist 3 (Compound 7) is a Nurr1 agonist (EC50: 0.07 μM). Nurr1 agonist 3 binds to the recombinant Nurr1 ligand binding domain (LBD) with a Kd value of 0.14 μM. Nurr1 agonist 3 increases the Nurr1-regulated genes tyrosine hydroxylase (TH) and vesicular amino acid transporter 2 (VMAT2) mRNA expression[1].
Phoyunnanin E, isolated from Dendrobium venustum, possesses anti-migration activity. Phoyunnanin E can be used for the research of cancer[1].
α7 Nicotinic receptor agonist-1 (Preparation 5) is an α7 nAChR agonist. α7 Nicotinic receptor agonist-1 can be used in studies of psychiatric disorders (such as schizophrenia, manic or hypomanic depression and anxiety disorders) and intellectual disorders (such as alzheimer's disease, learning deficits, cognitive deficits, attention deficits, memory loss, lewy body dementia and attention deficit hyperactivity disorder)[1].
Delavirdine(U 90152) is a potent non-nucleoside reverse transcriptase inhibitor (NNRTI).IC50 Value: 0.26 uM (Recombinant HIV-1 RT) [1]Target: HIV-1 reverse transcriptase; NNRTIin vitro: U-90152 [1-(5-methanesulfonamido-1H-indol-2-yl-carbonyl)-4-[3-(1-methyl eth yl-amino)pyridinyl]piperazine], which inhibited recombinant HIV-1 RT at a 50% inhibitory concentration (IC50) of 0.26 microM (compared with IC50s of > 440 microM for DNA polymerases alpha and delta). U-90152 blocked the replication in peripheral blood lymphocytes of 25 primary HIV-1 isolates, including variants that were highly resistant to 3'-azido-2',3'-dideoxythymidine (AZT) or 2',3'-dideoxyinosine, with a mean 50% effective dose of 0.066 +/- 0.137 microM. U-90152 had low cellular cytotoxicity, causing less than 8% reduction in peripheral blood lymphocyte viability at 100 microM. In experiments assessing inhibition of the spread of HIV-1IIIB in cell cultures, U-90152 was much more effective than AZT. When approximately 500 HIV-1IIIB-infected MT-4 cells were mixed 1:1,000 with uninfected cells, 3 microM AZT delayed the evidence of rapid viral growth for 7 days. In contrast, 3 microM U-90152 totally prevented the spread of HIV-1, and death and/or dilution of the original inoculum of infected cells prevented renewed viral growth after U-90152 was removed at day 24 [1]. Asdelavirdine concentration was increased from 0 to 100 microM, the K(M) for diclofenac metabolism rose from 4.5+/-0.5 to 21+/-6 microM, and V(max) declined from 4.2+/-0.1 to 0.54+/-0.08 nmol/min/mg of protein, characteristic of mixed-type inhibition [2].in vivo: The mean values (+/- standard deviations) for the maximum concentration in serum (C(max)) of ritonavir, the area under the concentration-time curve from 0 to 12 h (AUC(0-12)), and the minimum concentration in serum (C(min)) of ritonavir before the addition of delavirdine were 14.8 +/- 6.7 micro M, 94 +/- 36 micro M. h, and 3.6 +/- 2.1 micro M, respectively. These same parameters were increased to 24.6 +/- 13.9 micro M, 154 +/- 83 micro M. h, and 6.52 +/- 4.85 micro M, respectively, after the addition of delavirdine(P is <0.05 for all comparisons). Delavirdine pharmacokinetic parameters in the presence of ritonavir included a C(max) of 23 +/- 16 micro M, an AUC(0-8) of 114 +/- 75 micro M. h, and a C(min) of 9.1 +/- 7.5 micro M [3].Toxicity: Clinical trial: Quality of Life of HIV-infected Participants Switched to Raltegravir Versus Other Antiretroviral Regimens. Phase 4