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Naltrexone

  Cat. No.:  DC22472   Featured
Chemical Structure
16590-41-3
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More than 5000 active chemicals with high quality for research!
Field of application
A potent, competitive antagonist for μ, κ, δ, and σ-opioid receptors with Ki of 0.0825 nM, 0.509 nM, and 8.02 nM, for MOR, KOR, and DOR, respectively.
Cas No.: 16590-41-3
Chemical Name: Naltrexone
Synonyms: Naltrexone;17-(Cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinan-6-one;Naltrexone (base, anhydrous);Naltrexone solution;(5α)-17-(Cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinan-6-one;celupan;Depotrex;en1639;en1939;Naltrel;NeMexin;trexan;Trexonil;Um-792;C07253
SMILES: C1CC1CN2CC[C@@]34C5=C6C=CC(=C5O[C@H]4C(=O)CC[C@]3([C@H]2C6)O)O
Formula: C20H23NO4
M.Wt: 341.40092
Purity: 98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: A potent, competitive antagonist for μ, κ, δ, and σ-opioid receptors with Ki of 0.0825 nM, 0.509 nM, and 8.02 nM, for MOR, KOR, and DOR, respectively; also inhibits IL-6 and TNFα production in human immune cell subsets following stimulation with ligands for intracellular TLRs; a TLR-4 antognist that inhibits LPS-induced TLR4 downstream NO production in microglia BV-2 cells (IC50=105 uM).AlcoholismApproved
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
Cat. No. Product name Field of application
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DC75868 AZ14133346 AZ14133346 (compound 36) is a potent and selective inhibitor of EGFR Exon20 insertions, with the IC50 of 85 nM. AZ14133346 plays an important role in cancer research.
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DC74638 GLPG3667 GLPG3667 is an oral, reversible, and selective tyrosine kinase 2 (TYK2) inhibitor. It is being developed to treat inflammatory and auto-immune diseases. Biochemical assays showed that GLPG3667 displayed nanomolar potency on TYK2 with a selectivity over other JAK kinases >3-fold. In human PBMC, GLPG3667 showed comparable potency on the IFNα and IL-23 pathways (around 50 nM). Selectivity for TYK2 on the IFNα pathway was >14-fold and >19-fold toward the IL-2 and GM-CSF pathways in human PBMC and whole blood, respectively. Dermal ear inflammation in a mouse model of psoriasis driven by IL-23 was prevented by GLPG3667 with a minimal effective dose of 3 mg/kg given orally once daily. This effect was associated with a decrease in neutrophil infiltration and STAT3 phosphorylation at sites of inflammation. In healthy HV, GLPG3667 completely inhibited IFNα-induced STAT1 and STAT3 phosphorylation but did not impact IL-2- and GM-CSF-induced STAT5 phosphorylation.
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