AH-D peptide 

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^[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.

AH-D peptide (25 mg/kg, i.p., twice daily for 4 days) inhibits Zika virus-induced neuroinflammation and protects against Zika virus-induced neurodegeneration in IFN-α/β R^-/^- SV129 (A129^-/^-) mice^[1].
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-L1^EXO 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 CD4CD25 regulatory T cells and CD11bGr-1 myeloid and transforming growth factor-β (TGF-β)) with good tolerated (negligible changes in body weight and major organ histology, including heart, lung, liver, spleen, kidney, blood) in B16F10 tumour-bearing C57BL/6 mice^[2].
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.

3283.75

C₁₅₄H₂₂₈N₃₈O₄₀S

Solid

White to off-white

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}

d-{SGSWLRDVWDWICTVLTDFKTWLQSKL-NH2}

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* 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.

• [1]. Sol Shin, et al. Curvature-sensing peptide inhibits tumour-derived exosomes for enhanced cancer immunotherapy. Nat Mater. 2023 May;22(5):656-665.  [Content Brief]