66357-35-5 Usage
Description
Ranitidine, a H2-receptor agonist, caused contact
dermatitis within the pharmaceutical industry.
Uses
Different sources of media describe the Uses of 66357-35-5 differently. You can refer to the following data:
1. Antagonist (to histamine H2receptors).
2. It simultaneously reduces pepsin activity and is used for treating stomach
and duodenum ulcers as well as other conditions accompanied by elevated acidity of the gastrointestinal
tract. Synonyms of this drug are zantac, azantac, raniplex, ranidil, and others.
3. Ranitidine (cas# 66357-35-5) was used as a standard for testing the therapeutic effect of brown propolis extract against aspirin and ethanol- induced gastric ulcers.
Indications
Ranitidine (Zantac) is another H2 receptor antagonist that does not have the
same antiandrogen side effects as cimetidine. Note that both cimetidine and
ranitidine inhibit the cytochrome P-450 microsomal enzyme system.
General Description
Ranitidine, N-[2-[[[5-(dimethylamino)methyl]-2-furanyl]methyl]thiol] ethyl]-N'-methyl-2-nitro-l,1-ethenediamine (Zantac), is a white solid, which inits hydrochloride salt form is highly soluble in water. It is anaminoalkyl furan derivative with pKa values of 2.7 (sidechain) and 8.2 (dimethylamino). Ranitidine is more potentthan cimetidine, but less potent than famotidine. Likeother H2-antagonists, it does not appear to bind to otherreceptors.Bioavailability of an oral dose of ranitidine is about 50%and is not significantly affected by the presence of food.Some antacids may reduce ranitidine absorption and shouldnot be taken within 1 hour of administration of this drug. Theplasma half-life of the drug is 2 to 3 hours, and it is excretedalong with its metabolites in the urine. Three metabolites, ranitidineN-oxide, ranitidine S-oxide, and desmethyl ranitidine,have been identified. Ranitidine is only a weak inhibitor ofthe hepatic cytochrome isozymes, and recommended doses ofthe drug do not appear to inhibit the metabolism of otherdrugs. However, there have been isolated reports of drug interactions(warfarin, triazolam) that suggest that ranitidinemay affect the bioavailability of certain drugs by someunidentified mechanism, perhaps by pH-dependent effect onabsorption or a change in volume of distribution.In addition to being available in various dosage forms asthe hydrochloride salt, ranitidine is also available as a bismuthcitrate salt for use with the macrolide antibiotic clarithromycinin treating patients with an active duodenalulcer associated with H. pylori infection. Eradication of H.pylori reduces the risk of duodenal ulcer recurrence.
Biological Activity
Potent, selective and competitive histamine H 2 receptor antagonist (pA 2 = 6.95-7.2). In vivo, inhibits gastric acid secretion induced by histamine, pentagastrin, bethanecol and food. Also inhibits aspirin-induced gastric lesions.
Clinical Use
H2
antagonist:
Conditions associated with hyperacidity
Synthesis
Ranitidine, N[2-[[[5-[(dimethylamino)methyl]-2-furanyl]methyl]thio]ethyl]-
N′-methyl-2-nitro-1,1-ethendiamine (16.2.8), is synthesized from furfuryl alcohol, which
undergoes aminomethylation reaction using dimethylamine and paraform, which form 5-
(dimethylaminomethyl)furfuryl alcohol (16.2.6). Further reaction with 2-mercaptoethylamine
hydrochloride gives a product of substitution of the hydroxyl group in (16.2.6),
5-dimethylaminomethyl-2-(2′-aminoethyl)thiomethylfurane (16.2.7). Reacting this with Nmethyl-
1-methylthio-2-nitroethenaamine gives ranitidine (16.2.8).
Drug interactions
Potentially hazardous interactions with other drugs
Alpha-blockers: effects of tolazoline antagonised.
Antifungals: absorption of itraconazole and
ketoconazole reduced; concentration of posaconazole
possibly reduced - avoid.
Antivirals: concentration of atazanavir reduced;
concentration of raltegravir possibly increased - avoid;
avoid for 12 hours before and 4 hours after rilpivirine.
Ciclosporin: may increase or not change ciclosporin
levels; nephrotoxicity, additive hepatotoxicity and
thrombocytopenia reported.
Cytotoxics: reduced gefitinib concentration; reduces
concentration of erlotinib and possibly pazopanib,
give at least 2 hours before or 10 hours after
ranitidine; absorption of dasatinib reduced - avoid;
possibly reduced absorption of lapatinib.
Ulipristal: contraceptive effect possibly reduced -
avoid with high dose ulipristal.
Metabolism
Ranitidine is not extensively metabolised. A small
proportion of ranitidine is metabolised in the liver to
the N-oxide, the S-oxide, and desmethylranitidine; the
N-oxide is the major metabolite but accounts for only
about 4-6% of a dose.
The fraction of the dose recovered as metabolites is
similar after both oral and IV dosing; and includes 6%
of the dose in urine as the N-oxide, 2% as the S-oxide,
2% as desmethylranitidine and 1-2% as the furoic acid
analogue. There is also some excretion in the faeces.
Dosage forms
150 mg b.i.d.
Check Digit Verification of cas no
The CAS Registry Mumber 66357-35-5 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 6,6,3,5 and 7 respectively; the second part has 2 digits, 3 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 66357-35:
(7*6)+(6*6)+(5*3)+(4*5)+(3*7)+(2*3)+(1*5)=145
145 % 10 = 5
So 66357-35-5 is a valid CAS Registry Number.
InChI:InChI=1/C13H22N4O3S/c1-14-13(9-17(18)19)15-6-7-21-10-12-5-4-11(20-12)8-16(2)3/h4-5,9,14-15H,6-8,10H2,1-3H3/b13-9+
66357-35-5Relevant articles and documents
An improved synthesis of the antiulcer drug ranitidine from N-[2-[[[5- (hydroxymethyl)-2-furanyl]-methyl]-thio]-ethyl]-N'-methyl-2-nitro-1,1- ethenediamine
Aasen, Arne Jorgen,Skramstad, Jan
, p. 228 - 229 (1998)
An improved synthesis of the antiulcer drug ranitidine from N-[2-[[[5- (hydroxymethyl)-2-furanyl]-methyl]-thiol]-ethyl]-N'methyl-2-nitro-1,1- ethenediamine is reported.
New method for synthesizing ranitidine
-
Paragraph 0034; 0039-0044; 0047; 0052-0057; 0059; 0064-0069, (2018/12/14)
The invention discloses a new method for synthesizing ranitidine. The method comprises the steps of synthesizing vinylidene chloride, synthesizing 1, 1-dichloro-2-nitroethylene, carrying out a ring-closing reaction, carrying out a ring-opening reaction in presence of a desiccant, and synthesizing the ranitidine. The method adopts an anhydrous environment in the preparation process of a ring-opening product, thus avoiding the interference with the reaction and the generation of impurities due to the presence of water, reducing the post-treatment work and increasing the utilization rate of the raw materials. The preparation method provided by the invention effectively increases the reaction yield of the ring-opening product, improves the purity of the ring-opening reaction, and reduces the reaction time; therefore, the yield and purity of the product ranitidine are improved, the production cost is lowered, and the method is more beneficial to industrial production.
Critical Influence of 5-Hydroxymethylfurfural Aging and Decomposition on the Utility of Biomass Conversion in Organic Synthesis
Galkin, Konstantin I.,Krivodaeva, Elena A.,Romashov, Leonid V.,Zalesskiy, Sergey S.,Kachala, Vadim V.,Burykina, Julia V.,Ananikov, Valentine P.
, p. 8338 - 8342 (2016/07/19)
Spectral studies revealed the presence of a specific arrangement of 5-hydroxymethylfurfural (5-HMF) molecules in solution as a result of a hydrogen–bonding network, and this arrangement readily facilitates the aging of 5-HMF. Deterioration of the quality of this platform chemical limits its practical applications, especially in synthesis/pharma areas. The model drug Ranitidine (Zantac) was synthesized with only 15 % yield starting from 5-HMF which was isolated and stored as an oil after a biomass conversion process. In contrast, a much higher yield of 65 % was obtained by using 5-HMF isolated in crystalline state from an optimized biomass conversion process. The molecular mechanisms responsible for 5-HMF decomposition in solution were established by NMR and ESI-MS studies. A highly selective synthesis of a 5-HMF derivative from glucose was achieved using a protecting group at O(6) position.