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Principaux documents

SML3265

Sigma-Aldrich

DAPTA trifluoroacetate

≥95% (HPLC)

Synonyme(s) :

Adaptavir trifluoroacetate, D-Ala-Peptide T-NH2 trifluoroacetate, D-Ala-Peptide T-amide trifluoroacetate, Dala1-Peptide T-NH2 trifluoroacetate, Dala1-Peptide T-amide trifluoroacetate, H-D-Ala-STTTNYT-NH2 trifluoroacetate, H-D-Ala-Ser-Thr-Thr-Thr-Asn-Tyr-Thr-NH2 trifluoroacetate, [D-Ala1]-Peptide T-NH2 trifluoroacetate, [D-Ala1]-Peptide T-amide trifluoroacetate

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About This Item

Code UNSPSC :
51111800
Nomenclature NACRES :
NA.77

Niveau de qualité

100

Essai

≥95% (HPLC)

Forme

powder

Couleur

white to off-white

Température de stockage

−20°C

Actions biochimiques/physiologiques

DAPTA is a potent CCR5 antagonist, an amidated octapeptide corresponding to an HIV envelope glycoprotein gp120 (gp160)-derived sequence (aa 185-192; the SF-2 isolate) that competes against gp120-CD4 complex for interaction with CCR5 (IC50 = 0.42 nM against gp120CM235 binding to CCR5/CD4 cells, IC50 = 1.5/1.8 nM against gp120BaL/sCD4 or gp120CM235/sCD4 binding to CCR5+/CD4- cells). DAPTA blocks CCR5-dependent HIV host cell entry in cultures and in vivo.
Potent CCR5 antagonist that blocks CCR5-dependent HIV host cell entry in cultures and in vivo.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

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Certificats d'analyse (COA)

Lot/Batch Number

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Consulter la Bibliothèque de documents

Weiwei Yu et al.
Frontiers in pharmacology, 12, 551839-551839 (2021-05-07)
Background: Cigarette smoke exposure (CSE) is a major cause of chronic obstructive pulmonary disease (COPD). The smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the tight junction (TJ) proteins. Even though the inflammatory mechanism of chemokine (C-C motif)
Valeria Avdoshina et al.
AIDS (London, England), 34(7), 979-988 (2020-02-20)
Postmortem brains of patients diagnosed with HIV-1-associated neurocognitive disorders (HAND) exhibit loss of dendrites. However, the mechanisms by which synapses are damaged are not fully understood. Dendrite length and remodeling occurs via microtubules, the dynamics of which are regulated by
Ze Chen et al.
Cell death & disease, 12(2), 184-184 (2021-02-17)
The pathogenesis of bronchopulmonary dysplasia (BPD), involves inflammatory, mechanisms that are not fully characterized. Here we report that overexpression of C-C chemokine receptor 5 (CCR5) and its ligands is associated with BPD development. Lipopolysaccharide-induced BPD rats have increased CCR5 and

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