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SML2658

Sigma-Aldrich

TT-10

≥98% (HPLC)

Synonym(s):

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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About This Item

Empirical Formula (Hill Notation):
C11H10FN3OS2
CAS Number:
2230640-94-3
Molecular Weight:
283.35
UNSPSC Code:
12352200

Quality Level

100

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

2-8°C

SMILES string

NC1=C(C(C2=CC=C(S2)F)=O)SC(NCC=C)=N1

Biochem/physiol Actions

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

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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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