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184475-35-2

184475-35-2 Structure

184475-35-2 Structure
IdentificationMore
[Name]

Gefitinib
[CAS]

184475-35-2
[Synonyms]

AKOS 91371
GEFITINIB
IRESSA
n-(3-chloro-4-fluoro-phenyl)-7-methoxy-6-(3-morpholin-4-ylpropoxy)quinazolin-4-amine
N-(3-Chloro-4-fluorophenyl)-7-methoxy-6-[3-(4-morpholinyl)propoxy]-4-quinazolinamine
ZD 1839
4-Quinazolinamine, N-(3-chloro-4-fluorophenyl)-7-methoxy-6-[3-(4-morpholinyl)propoxy]-
Gefitinib(TINIBS)
6-(Benzyloxy)-7-methoxyquinazolin-4(3H)-one
Gefinitib
[Molecular Formula]

C22H24ClFN4O3
[MDL Number]

MFCD04307832
[Molecular Weight]

446.9
[MOL File]

184475-35-2.mol
Chemical PropertiesBack Directory
[Appearance]

Light-Yellow Crystalline Powder
[mp ]

119-1200C
[Usage]

An antineoplastic
[CAS DataBase Reference]

184475-35-2(CAS DataBase Reference)
Safety DataBack Directory
[HS Code ]

29349900
Questions And AnswerBack Directory
[Indications and Uses]

Gefitinib is an antineoplastic target therapy drug with relatively high specificity that was developed by the British pharmaceutical company AstraZeneca; it is the first molecular targeted drug to be used in non-small cell lung cancer treatment. Epidermal growth factors (EGF) are a kind of polypeptide with a relative molecular mass of 6.45x103, and they can bind with epidermal growth factor receptors (EGFR) on target cell membrane surfaces to trigger biological effects. EGFR is a type of tyrosine kinase (TK) type receptor, so when bound with EGF, it will promote TK activation in the receptor. This will cause tyrosine residue in the receptor to autophosphorylate and send continuous dividing signals into the cell, causing cell proliferation and differentiation. EGFR is abundant in human tissue, and it is highly expressed in malign tumors. Gefitinib blocks the signal transduction pathway of cell surface EGFR to prevent tumor growth, metastasis, and growth in blood vessels, and it can induce tumor cell apoptosis. Gefitinib is mainly used to treat non-stem cell lung cancer.
[Pharmacokinetics]

It is orally effective, with relatively slow absorption and metabolism following intake. The bioavailability of a single oral 250mg dose is nearly 60%, and its area under curve (AUC) is dependent on dosage. With single daily dosages, blood concentration is steady after 7-10 days, with blood concentration peaking 3-7 hours after medication and then gradually following biphasic reduction (its half-life is 12-58 hours, at an average of 28 hours). It is observed as dose-dependent pharmacokinetics, and following multiple dosages, AUC and Cmax increased proportionally. When taken with food, its Cmax and AUC did not decrease significantly. Its plasma protein binding rate is nearly 90%. Gefitinib is metabolized through many different pathways in the livers in a relatively complicated process; the main component of its oxidative metabolism is the cytochrome P450 enzyme CYP3A4, which mainly metabolizes O-Desmethyl metabolites. Metabolites are unrelated to the pharmacological effects of the original drug. The original drug and many metabolites are mostly passed through the biliary tract and excreted through feces, while the amount of drug excreted through urine is less than 4% the original dosage amount.
[Adverse Reactions]

Gefitinib is relatively well-tolerated, and most negative reactions are mild and reversible, characteristics that are vastly different from those of standard negative reactions to cytotoxic drugs. Common negative reactions include diarrhea, nausea, rashes, acne, vomiting, and feebleness. Only 1% of patients have had to cease treatment due to negative reactions with an occurrence rate over 20%. There have also been rare cases of acute interstitial pneumonia.
[Warnings and precautions]

Gefitinib is not suitable for pregnant women, and breastfeeding women should cease breastfeeding throughout their treatment period.
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