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SML2885

Sigma-Aldrich

Ac-SDKP trifluoroacetate

≥95% (HPLC)

Synonym(s):

Ac-SDKP-OH trifluoroacetate, Ac-Ser-Asp-Lys-Pro-OH trifluoroacetate, AcSDKP trifluoroacetate, Goralatide trifluoroacetate, N-acetyl-L-seryl-L-a-aspartyl-L-lysyl-L-proline trifluoroacetate, N-acetyl-Ser-Asp-Lys-Pro-OH trifluoroacetate, Thymosin ß4 (1-4) trifluoroacetate, Tß4 (1-4) trifluoroacetate

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About This Item

Empirical Formula (Hill Notation):
C20H33N5O9 · xC2HF3O2
CAS Number:
Molecular Weight:
487.50 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥95% (HPLC)

form

lyophilized powder

color

white to off-white

storage temp.

−20°C

Biochem/physiol Actions

Originally characterized as a "spleen colony-forming units (CFU-S) inhibitor" for its activity against hematopoietic pluripotent stem cell proliferation, Ac-SDKP (Goralatide) is an immunomodulatory and pro-angiogenic tetrapeptide derived from the N-terminal end of thymosin β4 (Tβ4 aa 1-4) via sequential enzymatic actions of meprin-α and prolyl-oligopeptidase (POP), while angiotensin converting enzyme (ACE) mediates Ac-SDKP degradation. In animal heart, kidney and brain injury studies, Ac-SDKP ameliorates end-organ damage by promoting angiogenesis, as well as by reducing inflammation and fibrosis.
Thymosin β4 (Tβ4)-derived immunomodulatory and pro-angiogenic peptide with in vivo anti-inflammatory and anti-fibrotic efficacy.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Lijuan Zhang et al.
Toxicology and applied pharmacology, 350, 1-10 (2018-04-24)
Damage to alveolar epithelial cells (AECs) caused by long-term inhalation of large amounts of silica dust plays a significant role in the pathology of silicosis. The present study was undertaken to investigate the regulatory mechanism(s) involved in type II AEC
Cesar A Romero et al.
American journal of physiology. Renal physiology, 316(1), F195-F203 (2018-11-08)
The antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is released from thymosin-β4 (Tβ4) by the meprin-α and prolyl oligopeptidase (POP) enzymes and is hydrolyzed by angiotensin-converting enzyme (ACE). Ac-SDKP is present in urine; however, it is not clear whether de novo tubular release
Umesh C Sharma et al.
Circulation. Heart failure, 11(8), e004867-e004867 (2018-10-26)
Advances in radiotherapy for thoracic cancers have resulted in improvement of survival. However, radiation exposure to the heart can induce cardiotoxicity. No therapy is currently available to inhibit these untoward effects. We examined whether a small tetrapeptide, N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), can

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