Home Apoptosis p53 inhibitor Pifithrin-α (PFTα) Hhydrobromide

연구용

Pifithrin-α (PFTα) Hhydrobromide p53 inhibitor

제품 번호: S2929

Pifithrin-α is an inhibitor of p53, inhibiting p53-dependent transactivation of p53-responsive genes. Pifithrin-α is also a potent agonist of the aryl hydrocarbon receptor (AhR).
Pifithrin-α (PFTα) Hhydrobromide p53 inhibitor Chemical Structure

화학 구조

분자량: 367.3

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품질 관리 (Quality Control)

배치: 순도: 99.87%
99.87

세포 배양, 처리 및 작업 농도
(Cell Culture, Treatment & Working Concentration)

세포주 분석 유형 농도 배양 시간 제형 활성 설명 PMID
mouse E15.5 cortical neurones Function assay Inhibition of death of mouse E15.5 cortical neurones
클릭하여 더 많은 세포주 실험 데이터 보기

화학 정보, 보관 및 안정성 (Chemical Information, Storage & Stability)

분자량 367.3 화학식

C16H18N2OS.HBr

 보관 (수령일로부터)
CAS 번호 63208-82-2 SDF 다운로드 원액 보관

동의어 Pifithrin-α hydrobromide Smiles CC1=CC=C(C=C1)C(=O)CN2C3=C(CCCC3)SC2=N.Br

용해도 (Solubility)

In vitro
배치:

DMSO : 73 mg/mL (198.74 mM)
(수분으로 오염된 DMSO는 용해도를 감소시킬 수 있습니다. 신선하고 무수 DMSO를 사용하십시오.)

Water : Insoluble

Ethanol : Insoluble

몰농도 계산기

질량 농도 부피 분자량
희석 계산기 분자량 계산기

In vivo
배치:

생체 내 제형 계산기 (투명한 용액)

1단계: 아래 정보 입력 (권장: 실험 중 손실을 고려하여 추가 동물 포함)

mg/kg g μL

2단계: 생체 내 제형 입력 (이것은 계산기일 뿐 제형이 아닙니다. 용해도 섹션에 생체 내 제형이 없는 경우 먼저 당사에 문의하십시오.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

계산 결과:

작업 농도: mg/ml;

DMSO 원액 준비 방법: mg 약물 사전 용해 μL DMSO ( 원액 농도 mg/mL, 농도가 해당 약물 배치의 DMSO 용해도를 초과하는 경우 먼저 당사에 문의하십시오. )

생체 내 제형 준비 방법: 취하다 μL DMSO 원액, 다음 추가μL PEG300, 혼합하고 투명하게 한 다음 추가μL Tween 80, 혼합하고 투명하게 한 다음 추가 μL ddH2O, 혼합하고 투명하게 합니다.

생체 내 제형 준비 방법: 취하다 μL DMSO 원액, 다음 추가 μL 옥수수 기름, 혼합하고 투명하게 합니다.

참고: 1. 다음 용매를 추가하기 전에 액체가 투명한지 확인하십시오.
2. 용매를 순서대로 추가해야 합니다. 다음 용매를 추가하기 전에 이전 추가에서 얻은 용액이 투명한 용액인지 확인해야 합니다. 와동, 초음파 또는 뜨거운 물 중탕과 같은 물리적 방법을 사용하여 용해를 도울 수 있습니다.

작용 메커니즘 (Mechanism of Action)

Targets/IC50/Ki
p53
시험관 내(In vitro)

Pifithrin-α inhibits p53-dependent transactivation of p53-responsive genes in ConA cells. Pifithrin-α (10 μM) inhibits apoptotic death of C8 cells induced by Dox, Taxol, cytosine arabinoside. Pifithrin-α inhibits p53-dependent growth arrest of human diploid fibroblasts in response to DNA damage but has no effect on p53-deficient fibroblasts. Pifithrin-α may modulate the nuclear import or export (or both) of p53 or may decrease the stability of nuclear p53. Pifithrin-α (100-200 nM) completely suppresses the camptothecin-induced increase in the level of p53 DNA binding as well as the p53-responsive gene Bax in hippocampal cell. Pifithrin-α also decreases the basal level of p53 DNA-binding activity. Pifithrin-α (200 nM) protects cultured hippocampal neurons against death induced by DNA-damaging agents. Pifithrin-α (200 μM) stabilizes mitochondrial function, suppresses caspase activation and protects cultured hippocampal neurons against death induced by glutamate and amyloid β-peptide. Pifithrin α, in addition to p53, can suppress heat shock and glucocorticoid receptor signaling but has no effect on nuclear factor-kappaB signaling. Pifithrin α (10 μM) reduces activation of heat shock transcription factor (HSF1) and increases cell sensitivity to heat. Pifithrin α (10 μM) reduces activation of glucocorticoid receptor and rescues mouse thymocytes from apoptotic death after treatment in HeLa cells. PFTalpha blocks p53-mediated induction of p21/Waf-1 in human embryonic kidney cells.

생체 내(In vivo)

Pifithrin-α (2.2 mg/kg i.p.) treatment completely rescues mice (C57BL and Balb/c) of both strains from 60% killing doses of gamma irradiation (8 Gy for C57BL and 6 Gy for Balb/c). Pifithrin-α-injected mice lost less weight than irradiated mice that are not pretreated with the Pifithrin-α. Pifithrin-α (2.2 mg/kg) abrogates p53-dependent regulation of DNA replication after whole-body gamma irradiation in mice. Pifithrin-α (2 mg/kg i.p.) 30 min prior to middle cerebral artery occlusion treatment of mice reduces ischemic brain injury and protects hippocampal neurons against excitotoxic injury. Pifithrin α (3.6 μg/kg i.p.) inhibits Dex-induced degeneration of the thymus in mice. Pifithrin α (2 mg/kg) results in a significantly lower degree of motor disability in rats receiving transient occlusion of the middle cerebral artery as compared with controls. Pifithrin α-treated animals has less motor disability and smaller infarcts when the drug is administered up to an hour after stroke onset. Pifithrin α results in significantly lower motor disability scores in rats than in the vehicle-treated animals at 7 days post-op. Pifithrin α results in significant reduction of apoptosis in rats as indicated by Tunel and caspase 3 staining.

참조
  • [4] https://pubmed.ncbi.nlm.nih.gov/15145929/
  • [5] https://pubmed.ncbi.nlm.nih.gov/15144874/

적용 분야 (Applications)

방법 바이오마커 이미지 PMID
Western blot p53 / p-PKCα / PKCα AMPK / p-AMPK / p-ACC / p27 / p53 FAK
S2929-WB1
26733200
Immunofluorescence LC3B LC3 / p-AMPK / p27
S2929-IF1
26733200