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BM0017

Sigma-Aldrich

BMS-199264 hydrochloride

≥98% (HPLC)

Synonym(s):

(3S,4R)-4-[(4-Chlorophenyl)(1H-imidazol-2-ylmethyl)amino]-3,4-dihydro-2,2-dimethyl-6-(1-piperidinylsulfonyl)-2H-1-Benzopyran-3-ol hydrochloride, (3S-trans)-1-[[4-[(4-Chlorophenyl)(1H-imidazol-2-ylmethyl)amino]-3,4-dihydro-3-hydroxy-2,2-dimethyl-2H-1-benzopyran-6-yl]sulfonyl]-piperidine monohydrochloride, BMS 199264 hydrochloride

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About This Item

Empirical Formula (Hill Notation):
C26H31ClN4O4S · HCl
CAS Number:
186180-83-6
Molecular Weight:
567.53
UNSPSC Code:
12352200
PubChem Substance ID:
329774360
NACRES:
NA.77
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Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 10 mg/mL, clear

storage temp.

room temp

SMILES string

O=S(C1=CC=C(OC(C)(C)[C@@H](O)[C@@H]2N(CC3=NC=CN3)C4=CC=C(Cl)C=C4)C2=C1)(N5CCCCC5)=O.[H]Cl

Biochem/physiol Actions

BMS-191264 decreases cardiac necrosis and improves the recovery of contractile activities after reperfusion.[1]
BMS-199624 is a potent inhibitor of the ATP hydrolase activity of mitochondrial F1F0 ATP synthase.
BMS-199624 is a potent inhibitor of the ATP hydrolase activity of mitochondrial F1F0 ATP synthase. The compound BMS-199624 has no affect on the ATP synthase function of F1F0. In isolated rat hearts, BMS-199624 blocks depletion of ATP levels, and blocks necrosis during ischemia.

Features and Benefits

BMS-199264 is available through a partnership with Bristol-Myers Squibb (BMS). To learn more and view other BMS compounds, visit sigma.com/BMS.

Legal Information

Sold for research purposes only under agreement from BMS.

Pictograms

Exclamation mark
GHS07

Signal Word

Warning

Hazard Statements

H315,H319,H335

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

Target Organs

Respiratory system

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

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Certificates of Analysis (COA)

Lot/Batch Number
096M4770V

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Gary J Grover et al.
Cardiovascular therapeutics, 26(4), 287-296 (2008-11-28)
The mitochondrial F1F0 ATP synthase is responsible for the majority of ATP production in mammals and does this through a rotary catalytic mechanism. Studies show that the F1F0 ATP synthase can switch to an ATP hydrolase, and this occurs under

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