CD4 (81-92) (human)
CD4 (81-92) (human) is a fragment of hCD4. CD4 (81-92) (human) can undergo structural modifications including derivatization and cyclization to enhance antiviral potency and stability, with sequence alterations affecting its activity. CD4 (81-92) (human) is applicable to studies related to HIV-1 infection.
For research use only. We do not sell to patients.
- CAS No.: 126144-46-5
- Formula: C62H96N14O26S
- Molecular Weight:1485.57
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
HIV-1 |
In Vitro
Derivatized CD4 (81-92) (human) peptides exhibit concentration-dependent anti-HIV infection, anti-syncytium formation and viral inhibitory activities in CEM-SS, VB and H9 cells, with their potency varying by derivatization pattern; cyclized W3 displays submicromolar activity, and peptides #18, #30 and W3 can also block SIVSMM-B670 infection of CEM-174 cells[1].
CD4 (81-92) (human) benzylated peptide (7.8-125 μM; administered only 0-48 h post-inoculation) potently inhibits infection of CEM-SS cells by HIV-1 (HTLV-IIIB) and HIV-1 (RF-II) within the first 48 hours of infection[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 126144-46-5
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Molecular Weight 1485.57
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Formula C62H96N14O26S
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SMILES
OC(C=C1)=CC=C1C[C@H](NC([C@@H](N)[C@H](O)C)=O)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](CS)C(N[C@@H](CCC(O)=O)C(N[C@@H](C(C)C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCCCN)C(N[C@@H](CCC(O)=O)C(N[C@H](C(O)=O)CCC(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O
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Sequence
Thr-Tyr-Ile-Cys-Glu-Val-Glu-Asp-Gln-Lys-Glu-Glu
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Sequence Shortening
TYICEVEDQKEE
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. Rausch DM, et al. CD4(81-92)-based peptide derivatives. Structural requirements for blockade of HIV infection, blockade of HIV-induced syncytium formation, and virostatic activity in vitro. Biochem Pharmacol. 1992 Apr 15;43(8):1785-96. [Content Brief]
[2]. Lifson JD, et al. Synthetic peptides allow discrimination of structural features of CD4(81-92) important for HIV-1 infection versus HIV-1-induced syncytium formation. AIDS research and human retroviruses. 1991 Jun;7(6):521-7. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)