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219007

Sigma-Aldrich

Caspase Inhibitor VI

Z-VAD-FMK, CAS 161401-82-7, is an irreversible pan caspase inhibitor. Does not require pretreatment with esterase for in vitro studies.

Synonym(s):

Caspase Inhibitor VI, Z-VAD-FMK

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About This Item

Empirical Formula (Hill Notation):
C21H28FN3O7
CAS Number:
Molecular Weight:
453.46
UNSPSC Code:
12352200

Quality Level

Assay

≥98% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated

color

off-white

solubility

DMSO: 9 mg/mL

shipped in

ambient

storage temp.

−20°C

InChI

1S/C21H28FN3O7/c1-12(2)18(25-21(31)32-11-14-7-5-4-6-8-14)20(30)23-13(3)19(29)24-15(9-17(27)28)16(26)10-22/h4-8,12-13,15,18H,9-11H2,1-3H3,(H,23,30)(H,24,29)(H,25,31)(H,27,28)/t13-,15-,18-/m0/s1

InChI key

SUUHZYLYARUNIA-YEWWUXTCSA-N

General description

An irreversible general caspase inhibitor. Useful for studies involving recombinant, isolated, and purified caspase enzymes. Unlike Caspase Inhibitor I (Cat. No. 627610), this inhibitor does not require pretreatment with esterase for in vitro studies. A 10 mM (1 mg/221 µl) solution of Caspase Inhibitor VI (Cat. No. 219011) in DMSO is also available.

Biochem/physiol Actions

Cell permeable: no
Product does not compete with ATP.
Reversible: no

Warning

Toxicity: Standard Handling (A)

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Wayne A Cabral et al.
Aging cell, 20(9), e13457-e13457 (2021-08-29)
Hutchinson-Gilford progeria syndrome (HGPS) is a rare accelerated aging disorder most notably characterized by cardiovascular disease and premature death from myocardial infarction or stroke. The majority of cases are caused by a de novo single nucleotide mutation in the LMNA
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Disease models & mechanisms, 14(11) (2021-10-09)
KCNQ4 encodes the homotetrameric voltage-dependent potassium ion channel Kv7.4, and is the causative gene for autosomal dominant nonsyndromic sensorineural hearing loss, DFNA2. Dominant-negative inhibition accounts for the observed dominant inheritance of many DFNA2-associated KCNQ4 variants. In addition, haploinsufficiency has been

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