제공된 대로 구매일로부터 1년 동안 안정적입니다. DMSO 용액은 -20°C에서 최대 3개월 동안 보관할 수 있습니다.
안전
위험 및 안전 성명
위험 및 사전주의 사항 (GHS)
WGK 독일
3
HS 번호
2934.20.8000
그림문자(GHS):
신호 어:
Warning
유해·위험 문구:
암호
유해·위험 문구
위험 등급
범주
신호 어
그림 문자
P- 코드
H302
삼키면 유해함
급성 독성 물질 - 경구
구분 4
경고
P264, P270, P301+P312, P330, P501
H315
피부에 자극을 일으킴
피부부식성 또는 자극성물질
구분 2
경고
P264, P280, P302+P352, P321,P332+P313, P362
H319
눈에 심한 자극을 일으킴
심한 눈 손상 또는 자극성 물질
구분 2A
경고
P264, P280, P305+P351+P338,P337+P313P
H335
호흡 자극성을 일으킬 수 있음
특정 표적장기 독성 - 1회 노출;호흡기계 자극
구분 3
경고
예방조치문구:
P261
분진·흄·가스·미스트·증기·...·스프레이의 흡입을 피하시오.
P305+P351+P338
눈에 묻으면 몇 분간 물로 조심해서 씻으시오. 가능하면 콘택트렌즈를 제거하시오. 계속 씻으시오.
Pifithrin-α (PFTα) C화학적 특성, 용도, 생산
개요
Pifithrin-α is an inactivator of p53 that blocks p53-dependent transcriptional activation and apoptosis. It prevents p53-mediated apoptosis induced by cytotoxic compounds in C8 cells at 10 μM and in human umbilical vein endothelial cells at 30 μM. Pifithrin-α can also protect cells from DNA damage-induced apoptosis by a p53-independent mechanism that might involve cyclin D1.
용도
Pifithrin-α has been used:
to study the effect of specific p53 inhibitor on p53-upregulated modulator of apoptosis (PUMA) expression after transient global cerebral ischemia (tGCI)
as p53 inhibitor to treat PA1 cells
as a tumor protein p53 (TRP53) inhibitor, to treat mouse lung epithelial-12 (MLE-12) cells
일반 설명
A cell-permeable chemical inhibitor of p53. Reversibly inhibits p53-dependent transactivation of p53-responsive genes and reversibly blocks p53-mediated apoptosis. Inhibits p53-dependent growth arrest of human diploid fibroblasts in response to DNA damage but has no effect on p53-deficient fibroblasts. Protects normal tissues from the deleterious side effects of chemotherapy. Has been reported to protect neurons against β-amyloid peptide and glutamate-induced apoptosis.
생물학적 활성
Inhibitor of p53; reversibly blocks p53-dependent transcriptional activation and apoptosis. Protects against neuronal death in models of stroke and neurodegenerative disorders. Active in vivo ; protects mice from the side-effects of cancer therapy associated with p53 induction. Potentially increases reprogramming efficiency of human somatic cells to induced pluripotent stem cells (iPSCs) by silencing p53. Also aryl hydrocarbon receptor (AHR) agonist, causes upregulation of AHR target gene CYP1A1 (EC 50 = 1.1 μ M).
