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Safety Information

SML2944

Sigma-Aldrich

Mca-YVADAPK(Dnp)-OH trifluoroacetate

≥97% (HPLC)

Synonym(s):

Mca-Tyr-Val-Ala-Asp-Ala-Pro-Lys(Dnp), TFA salt, Mca-Tyr-Val-Ala-Asp-Ala-Pro-Lys(Dnp)-OH, TFA salt, Mca-YVADAPK(Dnp), TFA salt (Mca = 7-Methoxycoumarin-4-yl; Dnp = 2,4-dinitrophenyl)

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About This Item

Empirical Formula (Hill Notation):
C53H64N10O19 · xC2HF3O2
Molecular Weight:
1145.13 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77
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Quality Level

100

Assay

≥97% (HPLC)

form

film or powder

color

white to dark beige

storage temp.

−20°C

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This Item
GE17089102GE17089109P4937
Percoll® Cytiva 17-0891-01, pack of 1 L

GE17089101

Percoll®

Percoll® Cytiva 17-0891-02, pack of 250 mL

GE17089102

Percoll®

Percoll® Cytiva 17-0891-09, pack of 6 × 1 L

GE17089109

Percoll®

Percoll® pH 8.5-9.5 (25 °C), suitable for cell culture

P4937

Percoll®

density

1.13 g/cm3

density

-

density

-

density

1.13 g/mL±0.005 g/mL at 25 °C (lit.)

packaging

pack of 1 L

packaging

pack of 250 mL

packaging

pack of 6 × 1 L

packaging

-

manufacturer/tradename

Cytiva 17-0891-01

manufacturer/tradename

Cytiva 17-0891-02

manufacturer/tradename

Cytiva 17-0891-09

manufacturer/tradename

-

color

Colorless to slightly yellow

color

Colorless to slightly yellow

color

Colorless to slightly yellow

color

-

pH range

8.5-9.5

pH range

8.5-9.5

pH range

8.5-9.5

pH range

-

Biochem/physiol Actions

Mca-YVADAPK(Dnp)-OH is a widely used fluorescent substrate for caspase-1 (ICE cleaves between D & A) and angiotensin-converting enzyme 2 (ACE2 cleaves between P & K). Proteolytic cleavage separates 7-methoxycoumarin-4-acetyl (Mca) from the fluorescence-quenching group 2,4-dinitrophenyl (Dnp), resulting in increased Mca fluorescence (Ex: 320-328 nm, Em: 405-420 nm).
Popular fluorescent substrate for caspase-1 (ICE) and angiotensin-converting enzyme 2 (ACE2).

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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    Certificates of Analysis (COA)

    Lot/Batch Number
    0000288347
    0000283747
    0000288347
    0000283747
    0000112157

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    Jiantao Song et al.
    Bioscience reports, 40(6) (2020-05-29)
    Angiotensin-converting enzyme 2 (ACE2) is considered as an endogenous negative regulator of renin-angiotensin system (RAS), exerting multiple cardiovascular protective roles. Whether mechanical stretch modulates ACE2 expression remains unknown. The present study aimed at investigating whether ACE2 is involved in physiological
    Erin B Bruce et al.
    Experimental gerontology, 111, 133-140 (2018-07-15)
    The obesity epidemic is multi-generational and is particularly debilitating in the aging population, necessitating the use of pharmaceutical interventions. Recent evidence suggests that increasing the activity of the angiotensin converting enzyme-2 [ACE2]/angiotensin-(1-7)[Ang-(1-7)]/Mas receptor (MasR) axis in obese animal models leads
    M Enari et al.
    Nature, 380(6576), 723-726 (1996-04-25)
    Binding of Fas ligand or an agonistic anti-Fas antibody induces apoptosis in Fas-bearing cells. The interleukin-1Beta-converting enzyme (ICE) is a cysteine protease that is involved in apoptosis induced by various stimuli, including Fas-mediated apoptosis. Several ICE homologues have been identified
    Chad Vickers et al.
    The Journal of biological chemistry, 277(17), 14838-14843 (2002-01-30)
    Human angiotensin-converting enzyme-related carboxypeptidase (ACE2) is a zinc metalloprotease whose closest homolog is angiotensin I-converting enzyme. To begin to elucidate the physiological role of ACE2, ACE2 was purified, and its catalytic activity was characterized. ACE2 proteolytic activity has a pH
    Chhinder P Sodhi et al.
    Journal of immunology (Baltimore, Md. : 1950), 203(11), 3000-3012 (2019-10-28)
    Angiotensin-converting enzyme 2 (ACE2) is a potent negative regulator capable of restraining overactivation of the renin-angiotensin system, which contributes to exuberant inflammation after bacterial infection. However, the mechanism through which ACE2 modulates this inflammatory response is not well understood. Accumulating

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