AH-D peptide
Based on 1 Customer Validation
AH-D peptide is a brain-penetrant antiviral agent disrupting highly curved lipid membranes. AH-D peptide exhibits broad-spectrum antiviral activity against ZIKV, Dengue virus, Chikungunya virus, yellow fever virus and Japanese encephalitis virus, with
IC50 values of 11.9, 12.5, 35.7, 206 and 136 nM, respectively. AH-D peptide reduces the viral load in the brain, suppresses inflammation, protects neurons, and does not damage the blood brain barrier. AH-D peptide restores antitumor immunity by decreasing circulating PD-L1+ exosomes, reducing intratumoral immunosuppressive cells (regulatory T cells, myeloid-derived suppressor cells), and enhancing T cell function. AH-D peptide inhibits membrane-enveloped viruses and cancer cell metastasis in vivo. AH-D peptide exhibits no immunogenicity and has negligible effects on normal tissues. AH-D peptide can be used for research in Zika virus and other mosquito-borne viruses, cancer immunotherapy and metastasis.
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- Purity: 99.32%
- 화학식: C154H228N38O40S
- 분자량:3283.75
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보관:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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용액&용해도
- 순도&문서
- References
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Help & FAQs
Biological Activity
IC50 values of 11.9, 12.5, 35.7, 206 and 136 nM, respectively. AH-D peptide reduces the viral load in the brain, suppresses inflammation, protects neurons, and does not damage the blood brain barrier. AH-D peptide restores antitumor immunity by decreasing circulating PD-L1+ exosomes, reducing intratumoral immunosuppressive cells (regulatory T cells, myeloid-derived suppressor cells), and enhancing T cell function. AH-D peptide inhibits membrane-enveloped viruses and cancer cell metastasis in vivo. AH-D peptide exhibits no immunogenicity and has negligible effects on normal tissues. AH-D peptide can be used for research in Zika virus and other mosquito-borne viruses, cancer immunotherapy and metastasis[1][2].
AH-D peptide (50-1000 nM) induces liposome rupture at 50 nM, with the rupture time shortening as the concentration increases (50-1000 nM)[1].
AH-D peptide (100 nM) preferentially targets small liposomes (≤ 300 nm)[1].
AH-D peptide (10-500 nM, 48 h) effectively protects primary neuronal cell cultures against cell death induced by the ZIKV MR766 strain[1].
AH-D peptide (10-500 nM, 48 h) inhibits viral replication, protects against ZIKV-induced neuronal cell death, and suppresses replication of the contemporary ZIKV strain HS-2015-BA-01[1].
AH-D peptide shows antiviral activity against ZIKV, Dengue virus, Chikungunya virus, yellow fever virus and Japanese encephalitis virus, with IC50 values of 11.9, 12.5, 35.7, 206 and 136 nM, respectively[1].
AH-D peptide can disrupt T-EXOs and exhibits pH-enhanced membrane disruption (at acidic pH (6.5/6.8) than at neutral pH (7.4)) under acidic conditions relevant to the TME[2].
AH-D peptide (3 μM, 10 min) results in loss of PD-L1EXO-binding capacity to T cells and prevents T-EXO-mediated T cell exhaustion in T-EXOs[2].
AH-D peptide (1-6 h) significantly decreases T cell uptake of T-EXOs[2].
AH-D peptide results significantly greater proliferative potential in T cells, prevents T-EXOs from inhibiting the cytotoxic functions of activated T cells[2].
AH-D peptide has an appreciably higher fraction of gran zyme B (Grz-B)-expressing CD8+ T cells and greater production of pro-inflammatory cytokines, namely interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) [2].
AH-D peptide is mainly related to T-EXO depletion rather than tumouricidal activity, indicating by a negligible effect on the membrane permeability and viability of B16F10 melanoma cells in cytotoxicity test[2].
AH-D peptide effectively reshaped the local TME towards an ICB-sensitive phenotype and inhibited both fibrosis and angiogenesis[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:primary neuronal cell
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Concentration:10, 50, 100, 300, 500 nM
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Incubation Time:48 h
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Result:Results: prevented neuronal cell death and exhibited no toxicity to uninfected cells.
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Cell Line:plasma from B16F10 tumor-bearing mice
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Concentration:3 μM
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Incubation Time:10 min
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Result:Resulted a reduction of binding capacity of the T-EXOs.
AH-D peptide (25 mg/kg ) reduces the viral load in the brain by more than 1 log₁₀ and does not alter the integrity or permeability of the blood-brain barrier in A129-/- mice (before intracranially inoculated p.f.u of the ZIKV HS-2015-BA-01 strain 2×105)[1].
AH-D peptide (7.5 mg/kg, s.c., 6 times) markedly reduced binding capacity of the T-EXOs in PD-L1-bearing T-EXOs isolated from the plasma of B16F10 tumour-bearing mice[2].
AH-D peptide (0-7.5 mg/kg, i.t., 16 days) monotherapy decreases circulating PD-L1EXO levels with a reduction of up to 76% in B16F10 tumour-bearing C57BL/6 mice[2].
AH-D peptide (7.5 mg/kg, i.t., 21 days) significantly diminishes the intratumoural populations of immunosuppressive cells (including CD4
AH-D peptide (7.5 mg/kg, s.c., 4-10 days) exerts no peptide-induced immunogenicity or immunological memory in Wild-type (WT) C57BL/6 mice[2].
AH-D peptide (7.5 mg/kg, i.t.,) demonstrates the superior anti-tumour efficacy when combination with aPD-1 (5 mg/kg, i.p.) in B16F10 tumour-bearing C57BL/6 mice, showing an appreciably larger reductions in tumour volume and weight (80%) but negligible change in tumour growth without aPD-1[2].
AH-D peptide exerts potent anti-metastatic effects by targeting and disrupting T-EXOs, thereby blocking T-EXOs-mediated lung/liver metastasis and premetastatic niche formation in B16F10 tumor-bearing mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:IFN-α /β R-/- SV129 (A129-/-) mice (7-9 weeks) treat with plaque-forming units (p.f.u) of the ZIKV HS-2015-BA-01 strain (i.v., 4 × 103)[1]
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Dosage:25 mg/kg
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Administration:i.p., twice daily for 4 days
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Result:Protected 10 out of 12 infected mice from virus-induced mortality.
Alleviated ZIKV-induced weight loss in infected mice and maintained intraocular pressure at baseline levels.
Significantly reduced total and differential leukocyte counts.
Significantly decreased viral loads in the serum, spleen, brain, and optic nerve.
Reduced serum viraemia by > 1 log₁₀ and viral loads in the spleen and brain by > 2 log₁₀ at day 4 post-infection Reduced viral load in the brain by > 3 log₁₀ at day 4 post-infection with most significate effects.
Reduced viral load in the brain, which was associated with a significant decrease in myeloperoxidase (MPO) activity in the brain, indicating diminished leukocyte recruitment.
Markedly reduced the levels of cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), as well as chemokines including CCL5 and CXCL-1 in the brain.
Protected against ZIKV-induced cerebral damage.
Prevented leukocyte infiltration into the meninges.
Significantly reduced microglial activation in the motor cortex and hippocampus.
Chemical Information
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Appearance Solid
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분자량 3283.75
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화학식 C154H228N38O40S
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Color White to off-white
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Sequence
d-{Ser-Gly-Ser-Trp-Leu-Arg-Asp-Val-Trp-Asp-Trp-Ile-Cys-Thr-Val-Leu-Thr-Asp-Phe-Lys-Thr-Trp-Leu-Gln-Ser-Lys-Leu-NH2}
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Sequence Shortening
d-{SGSWLRDVWDWICTVLTDFKTWLQSKL-NH2}
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
용액&용해도
DMSO : 100 mg/mL (30.45 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
순도&문서
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Data Sheet (287 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
References
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 0.3045 mL | 1.5226 mL | 3.0453 mL | 7.6132 mL |
| 5 mM | 0.0609 mL | 0.3045 mL | 0.6091 mL | 1.5226 mL | |
| 10 mM | 0.0305 mL | 0.1523 mL | 0.3045 mL | 0.7613 mL | |
| 15 mM | 0.0203 mL | 0.1015 mL | 0.2030 mL | 0.5075 mL | |
| 20 mM | 0.0152 mL | 0.0761 mL | 0.1523 mL | 0.3807 mL | |
| 25 mM | 0.0122 mL | 0.0609 mL | 0.1218 mL | 0.3045 mL | |
| 30 mM | 0.0102 mL | 0.0508 mL | 0.1015 mL | 0.2538 mL |
AH-D peptide Related Classifications
HY-P10862 Related Classifications
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