SML2658
TT-10
≥98% (HPLC)
동의어(들):
N2-Allyl-5-[(5-fluorothiophen-2-yl)carbonyl]thiazole-2,4-diamine, TAZ K, TAZ-K, TT 10, [4-Amino-2-(2-propen-1-ylamino)-5-thiazolyl](5-fluoro-2-thienyl)methanone
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모든 사진(1)
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5 MG
₩169,201
25 MG
₩682,283
About This Item
실험식(Hill 표기법):
C11H10FN3OS2
CAS Number:
Molecular Weight:
283.35
UNSPSC 코드:
41106609
NACRES:
NA.77
추천 제품
Quality Level
분석
≥98% (HPLC)
양식
powder
색상
white to beige
solubility
DMSO: 2 mg/mL, clear
저장 온도
2-8°C
SMILES string
NC1=C(C(C2=CC=C(S2)F)=O)SC(NCC=C)=N1
InChI
1S/C11H10FN3OS2/c1-2-5-14-11-15-10(13)9(18-11)8(16)6-3-4-7(12)17-6/h2-4H,1,5,13H2,(H,14,15)
InChI key
GVYPHJQPOHDZEI-UHFFFAOYSA-N
생화학적/생리학적 작용
TAZ activator that promotes cardiomyocytes proliferation by activating YAP/TEAD-mediated transcription, as well as by exerting antioxidant and antiapoptotic activity.
TT-10 (TAZ K) is a TAZ (transcriptional coactivator with PDZ-binding motif) activator that promotes cardiomyocytes (CMs) proliferation (fold-increase by 10 μM TT-10 over untreated control = 5.2/rat CMs/40 hrs & 2.6/human iPSC-derived CMs/48 hrs) by activating YAP (YES-associated protein)/TEAD (transcriptional enhancer factor domain) complex-mediated transcription, as well as by exerting antioxidant and antiapoptotic activity. TT-10 ameliorates myocardial infarction-induced cardiac dysfunction in mice in vivo (10 mg/kg i.p.) at least in part via enhancing clonal expansion of existing cardiomyocytes with nuclear YAP expression.
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
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시험 성적서(COA)
Lot/Batch Number
Hironori Hara et al.
JACC. Basic to translational science, 3(5), 639-653 (2018-11-21)
Accumulating data suggest that new cardiomyocytes in adults are generated from existing cardiomyocytes throughout life. To enhance the endogenous cardiac regeneration, we performed chemical screenings to identify compounds that activate pro-proliferative YES-associated protein and transcriptional enhancer factor domain activities in
Masamichi Ito et al.
Journal of molecular and cellular cardiology, 128, 90-95 (2019-01-27)
Since regenerative capacity of adult mammalian myocardium is limited, activation of the endogenous proliferative capacity of existing cardiomyocytes is a potential therapeutic strategy for treating heart diseases accompanied by cardiomyocyte loss. Recently, we performed a compound screening and developed a
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