Ph-Ph+
Ph-Ph+ is a hemiprotonic compound, which is produced from phenanthroline (ph) dimerization. Ph-Ph+ has antitumor, antibacterial and antifungal activities.
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- 화학식: C24H17N4+
- 분자량:361.42
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
In Vitro
Ph-Ph+ (0.0039-2 μmol/mL; 24-72 hours) inhibits the various tumor cell proliferation in a concentration- and time-dependent manner for H22, U251MG, human neuroblastoma SH-SY5Y cell line, mouse melanoma B16 cell line, and human lung adenocarcinoma A549 cell line). , Ph-Ph+ does not affect the viabilities of human L02 cells and HUVEC cells. Under an optical microscope, Ph-Ph+-treated tumor cells shrank and exhibited apoptotic bodies. Ph-Ph+ has a selective antitumor effect through inducing cell apoptosis[1].
Ph-Ph+ has broad-spectrum antibacterial and antifungal activities, and drug-resistant bacteria, including methicillin-resistant Staphylococcus aureus[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
In animal models of liver cancer with fungal infection, the Ph-Ph+ (2-8 mg/kg; i.v; once a day for 9 days) retards proliferation of hepatoma cells in tumor-bearing mice and remedies pneumonia and encephalitis caused by Cryptococcus neoformans[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Chemical Information
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분자량 361.42
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화학식 C24H17N4+
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SMILES
C12=C(C=CC3=C2[N+]([H][N]4=CC=CC5=C4C6=C(C=CC=N6)C=C5)=CC=C3)C=CC=N1
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)