ifindCPcli

ifindCPcli identifies chokepoint reactions in genome-scale metabolic models to pinpoint reactions whose inhibition or alteration can perturb cellular metabolism and inform drug-target discovery.

Key Features:

• Chokepoint Computation: Identifies chokepoint reactions by analyzing network topology together with dynamic flux distributions.
• Dead-End Metabolite Removal: Detects and removes dead-end metabolites that do not contribute to downstream reactions in the model.
• Essential Reaction Identification: Identifies reactions essential for maintaining cellular functions within the metabolic network.
• Flux Bound Updates (FVA): Updates reaction flux bounds based on Flux Variability Analysis (FVA) results.
• Input and Output Formats: Accepts SBML files as input and exports results in a spreadsheet format detailing chokepoint computations and analyses.
• Integrated Host-Pathogen Modeling: Enables integration of human cellular metabolism with pathogen-specific processes for comparative analysis.

Scientific Applications:

• Drug Target Identification: Supports identification of unique biochemical reactions as potential drug targets in integrated human–viral metabolic models, including SARS-CoV-2 studies.
• Pathogenic Mechanism Insights: Facilitates modeling of SARS-CoV-2–human cell interactions to reveal virus-induced alterations in cellular functions related to disease progression and cell death.
• Therapeutic Strategy Support: Informs studies of viral entry inhibition, immune regulation, and drug optimization to support therapeutic strategy development.

Methodology:

Performs chokepoint computation using both network topology and dynamic flux distributions, identifies and removes dead-end metabolites, updates flux bounds via Flux Variability Analysis (FVA), and supports integrated modeling of human cellular metabolism with pathogen-specific processes for comparative analysis of healthy and infected states.