기본 정보
- CAS
775304-57-9- 표준 SMILES
O=C(O)c1cccc(-c2noc(-c3ccccc3F)n2)c1- InChIKey
OOUGLTULBSNHNF-UHFFFAOYSA-N- 분자식
- C15H9FN2O3
- 평균 분자량
- 284.24 g/mol
- 단동위원소 질량
- 284.05972037
개요
3-[5-(2-fluorophenyl)-1,2,4-oxadiazol-3-yl]benzoic acid is a ring assembly and an oxadiazole.
이름 및 식별자
- 우선 이름
- Ataluren
- IUPAC
- 3-[5-(2-fluorophenyl)-1,2,4-oxadiazol-3-yl]benzoic acid
- 영어명
- Ataluren
- 분자식
- C15H9FN2O3
- 분자량
- 284.24
이름 및 동의어
이름 더 보기
데이터베이스 식별자
- CAS
775304-57-9- PubChem CID
- 11219835
- DTXSID
DTXSID5046776- ChEMBL
CHEMBL256997- ChEBI
CHEBI:94805- UNII
- K16AME9I3V
- EC Number
- 695-053-5、922-364-8
- Nikkaji
- J2.446.661B
물성
구조 계산 물성
- XLogP
- 3.1
- 극성 표면적
- 76.2 Ų
- 수소 결합 공여자 수
- 1
- 수소 결합 수용자 수
- 6
- 회전 가능 결합 수
- 3
- 무거운 원자 수
- 21
- 형식 전하
- 0
- 복잡도
- 382
실험 및 물리화학적 성질
Drugs
Pharmaceuticals -> Musculo-skeletal system -> Other drugs for disorders of the musculo-skeletal system
Pharmaceuticals -> Listed in ZINC15
물리화학적 성질
- 녹는점
- 241 · 241 - 242°C
- 끓는 점
- 503.7 · 503.7±60.0 °C(Predicted)
- 밀도
- 1.379 · 1.379
- 저장 조건
- Refrigerator
- 용해도
- DMSO (약간 용해됨)
- 물리적 상태
- 흰색 내지 회백색 고체.
- 산도 계수 (pKa)
- 3.58 · 3.58±0.10(Predicted)
- 색상
- 흰색에서 황백색까지
- InChI
- InChI=1S/C15H9FN2O3/c16-12-7-2-1-6-11(12)14-17-13(18-21-14)9-4-3-5-10(8-9)15(19)20/h1-8H,(H,19,20)
- InChIKey
- OOUGLTULBSNHNF-UHFFFAOYSA-N
- SMILES
- C(O)(=O)C1=CC=CC(C2N=C(C3=CC=CC=C3F)ON=2)=C1
안전 및 규제
GHS 분류
GHS Classification
This chemical does not meet GHS hazard criteria for 100% (2 of 2) of all reports.
Not Classified
Aggregated GHS information provided per 2 reports by companies from 1 notifications to the ECHA C&L Inventory.
유해성 정보
안전 데이터
- wgk
- WGK 3
- HS 번호
- 2933998090
- Hazard Classifications
- STOT RE 2STOT SE 3
- 스토리지 클래스
- 11 - Combustible Solids
화학 및 산업
약리 정보
ATC Code
M - Musculo-skeletal system
QM - Musculo-skeletal system
Mechanism of Action
Ataluren enables ribosomal readthrough of mRNA containing premature stop codons that otherwise would result in premature termination of protein chains. Use of ataluren allows cellular machinery to bypass nonsense mutations in genetic material, continue the translation process, and thereby restore the production of a full-length, functional protein. The research on the effects of Ataluren on the translation and stability of nonsense-containing mRNA in vitor show that Ataluren promoted readthrough at each of the nonsense codons, showing maximal activity with UGA, while having no effect on mRNA levels. Unlike the stable cell line assays, Ataluren did not discriminate significantly between the UAG and UAA mRNAs. Ataluren was a more potent nonsense-suppressing agent than gentamicin, and exhibited 4- to 15-fold stimulation of in vitro readthrough relative to the controls at levels similar to those in the stable cell reporter assays. These results indicate that Ataluren modulates termination efficiency at premature nonsense codons.
Metabolism/Metabolites
Ataluren is metabolized by conjugation via uridine diphosphate glucuronosyltransferase (UGT) enzymes, predominantly UGT1A9 in liver and intestine. In vivo, the only metabolite detected in plasma after oral administration of radio-labelled ataluren was the ataluren-O-1β-acyl glucuronide; exposure to this metabolite in humans was approximately 8% of the plasma AUC of ataluren.
Absorption, Distribution and Excretion
Peak plasma levels of ataluren are attained approximately 1.5 hours after dosing in subjects who received medicinal product within 30 minutes of a meal.
After a single oral dose of radiolabeled ataluren, approximately half of the administered radioactive dose is recovered in the faeces and the remainder was recovered in the urine. In the urine, unchanged ataluren and the acyl glucuronide metabolite account for less than 1% and 49%, respectively, of the administered dose.
응용 분야
개요Ataluren is a drug marketed under the trade name Translarna® which was developed by PTC Therapeutics and approved by the European Union in May 2014 for the treatment of Duchenne’s muscular dystrophy (DMD) and potentially other genetic disorders. Ataluren renders ribosomes less sensitive to premature stop or ‘read-through’ codons, which are thought to be beneficial in diseases such as DMD and cystic fibrosis.
용도Nonsense mutations create a premature termination of mRNA translation and have been implicated in various genetic disorders, including muscular dystrophy and cystic fibrosis. PTC-124 is a nonaminoglycoside that has been reported to selectively induce ribosomes to read through premature nonsense stop signals on mRNA, thus allowing the production of full-length, functional proteins. In a mouse model of cystic fibrosis caused by nonsense mutations, PTC-124 treatment (60 mg/kg s.c. injection or 0.3-0.9 mg/ml orally) has been shown to restore cystic fibrosis transmembrane conductance regulator (CFTR) protein expression and function. The target activity of PTC-124 was initially evaluated by firefly luciferase reporter cell-based nonsense codon assay (IC50 = 7 nM); however, subsequent assessments using a Renilla reniformis luciferase reporter have failed to produce nonsense codon suppression activity. Thus, while PTC-124 is in clinical testing in patients with nonsense mutations within the CFTR or dystrophin genes, controversy surrounds its exact mechanism of action.[Cayman Chemical]
상·하류 제품 정보
상류 원료
공급사100 곳
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