DA 4643 dihydrochloride
DA 4643 (hydrochloride) is an H2 receptor antagonist with the chemical name 2-guanidino-4 (3-methylaminomethyleneiminophenyl) thiazole dihydrochloride. It has a weak interaction with cytochrome P-450 and has a less inhibitory effect on P-450 than cimetidine and tiotidine. DA 4643 (hydrochloride) is able to inhibit both enzymatic and non-enzymatic lipid peroxidation reactions. This inhibition may not be achieved by inhibiting agent metabolizing enzymes, but rather due to the antioxidant properties of the compound itself. Compared with other H2 receptor antagonists such as cimetidine, ranitidine and tiotidine, DA 4643 (hydrochloride) shows a unique effect in lipid peroxidation inhibition. These properties make DA 4643 (hydrochloride) a potential H2 receptor antagonist with multiple mechanisms of action.
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- CAS No.: 95833-19-5
- Formule: C12H16Cl2N6S
- Masse moléculaire:347.27
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
Description
Chemical Information
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CAS No. 95833-19-5
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Masse moléculaire 347.27
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Formule C12H16Cl2N6S
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SMILES
C/N=C/NC1=CC=CC(C2=CSC(NC(N)=N)=N2)=C1.Cl.Cl
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)