Peniterphenyl A
Peniterphenyl A is a natural product obtained from a deep-sea-derived Penicillium sp. Peniterphenyl A inhibits HSV-1/2 virus entry into cells and may block HSV-1/2 infection through direct interaction with virus envelope glycoprotein D to interfere with virus adsorption and membrane fusion. Peniterphenyl A is a promising lead compound against HSV-1/2.
For research use only. We do not sell to patients.
- CAS No.: 2864816-15-7
- Formula: C19H14O6
- Molecular Weight:338.31
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
-
Biological Activity
-
Chemical Information
- Protocols
- Purity & Documentation
- References
-
Help & FAQs
Biological Activity
Description
IC50 & Target
|
HSV-1 |
Cellular Effect
|
Cell Line
|
Type | Value | Description | References |
|---|---|---|---|---|
| Vero | CC50 |
>100 μM
Compound: 1
|
Cytotoxicity against African green monkey Vero cells assessed as reduction in cell viability incubated for 3 days by MTT assay
Cytotoxicity against African green monkey Vero cells assessed as reduction in cell viability incubated for 3 days by MTT assay
|
[PMID: 34766503] |
Chemical Information
-
CAS No. 2864816-15-7
-
Molecular Weight 338.31
-
Formula C19H14O6
-
SMILES
COC1=C(C2=C(OC3=C2C=C(C(O)=C3)O)C=C1C4=CC=C(C=C4)O)O
-
Structure Classification
-
Initial Source
deep-sea-derived Penicillium sp. SCSIO41030
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Peniterphenyl A Related Classifications
HY-N10177 Related Classifications
Powered by Bioz