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SML2627

Sigma-Aldrich

Connexin43 mimetic peptide 5 trifluoroacetate salt

≥95% (HPLC)

Synonym(s):

Peptide 5 trifluoroacetate salt, VDCFLSRPTEKT trifluoroacetate salt, Val-Asp-Cys-Phe-Leu-Ser-Arg-Pro-Thr-Glu-Lys-Thr trifluoroacetate salt

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About This Item

Empirical Formula (Hill Notation):
C60H98N16O20S · xC2HF3O2
CAS Number:
Molecular Weight:
1395.58 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.77

assay

≥95% (HPLC)

form

lyophilized powder

color

white to beige

storage temp.

−20°C

Biochem/physiol Actions

Connexin43 mimetic peptide 5 is a blocker of connexin43 hemichannels that inhibits gap junction channels following CNS injury. Peptide 5 was designed to bind to extracellular regions of the connexin43 protein.

Storage Class

13 - Non Combustible Solids

wgk_germany

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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Yilin Mao et al.
Experimental brain research, 235(10), 3033-3048 (2017-07-21)
Systemic administration of a Connexin43 mimetic peptide, Peptide5, has been shown to reduce secondary tissue damage and improve functional recovery after spinal cord injury (SCI). This study investigated safety measures and potential off-target effects of Peptide5 systemic administration. Rats were
Yeri Kim et al.
Biochimica et biophysica acta. General subjects, 1861(2), 68-78 (2016-11-07)
Non-selective Connexin43 hemichannels contribute to secondary lesion spread. The hemichannel blocking peptidomimetic Peptide5, derived from the second extracellular loop of the human Connexin43 protein, prevents lesion spread and reduces vascular permeability in preclinical models of central nervous system injury. The
Helen V Danesh-Meyer et al.
Brain : a journal of neurology, 135(Pt 2), 506-520 (2012-02-22)
Connexin43 gap junction protein is expressed in astrocytes and the vascular endothelium in the central nervous system. It is upregulated following central nervous system injury and is recognized as playing an important role in modulating the extent of damage. Studies

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