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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5440_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Computational Methods for Rational Drug Design
- •Contents
- •1.1.2.2 GROMACS
- •1.1.2.3 Amber
- •1.1.2.4 CHARMM
- •1.1.2.5 AutoDock
- •1.1.2.6 VMD
- •1.1.2.7 PyMOL
- •1.1.2.8 Open Babel
- •List of Contributors
- •Preface
- •1. Molecular Modeling and Drug Design
- •1.1 Introduction
- •1.1.1 What Is Molecular Modeling?
- •1.1.2 Software Used for Molecular Modeling
- •1.1.2.1 Schrodinger
- •1.1.2.9 Avogadro
- •1.1.2.10 Discovery Studio
- •1.1.3 Molecular Mechanics
- •1.1.3.1 Prediction of Binding Affinity
- •1.1.3.2 Conformational Analysis
- •1.1.3.3 Virtual Screening
- •1.1.3.4 Lead Discovery
- •1.1.3.5 Mechanism of Action
- •1.2 Types of Molecular Models
- •1.2.1 Ball-and-Spoke Model
- •1.2.1.1 Future Directions
- •1.2.2 Space-filling Models
- •1.2.2.1 Future Directions
- •1.2.3 Crystal Lattice Models
- •1.2.3.1 Future Directions
- •1.3 Computational Methods in Drug Discovery
- •1.3.1 What Is Drug Discovery?
- •1.3.2 Computational Platforms for Drug Discovery
- •1.3.2.1 NCBI
- •1.3.2.2 Chemical Databases
- •1.3.2.3 PDB
- •1.3.2.5 UniProt
- •1.3.2.6 QSAR
- •1.3.2.8 Desmond
- •1.3.2.9 OpenBabel
- •1.3.2.10 DeepChem and Cheminformatics for Python (RDKit)
- •1.3.2.11 SBML
- •1.3.2.12 Virtual Screening
- •1.3.3 Applications of Computer-Based Methods in Steps of Drug Discovery
- •1.4 Potential Use and Application of AI in Drug Designing
- •1.4.1 Target Identification and Validation
- •1.4.2 Drug Screening and Lead Optimization
- •1.4.3 De Novo Drug Design
- •1.4.4 Predictive Toxicology and ADMET
- •1.4.5 Clinical Trial Optimization
- •1.4.6 Drug Repurposing
- •1.4.7 Concept of Personalized Medicine
- •1.4.8 Drug Combination Optimization
- •1.5 Limitations of Current Methods
- •1.5.1 Data Restrictions
- •1.5.2 Interpretability
- •1.5.3 Generalization
- •1.5.4 Resources and Computation
- •1.5.5 Ethical Considerations
- •1.5.6 Validation and Experimentation
- •1.5.7 Regulatory Obstacles
- •1.6 Case Studies
- •1.7 Molecular Docking
- •1.7.1 What Is Molecular Docking?
- •1.7.1.1 Procedure
- •1.7.1.2 Biophysical Laws
- •1.7.1.3 Rigid and Flexible Docking
- •1.7.1.4 Types of Docking
- •1.7.1.5 Challenges and Future Perspectives
- •1.7.2 Applications of Molecular Docking in Drug Designing
- •1.7.3 Success of Molecular Docking Cases in Drug Designing
- •1.8 Conclusion and Future Works
- •References
- •2. Bioactive Small Molecules and Drug Discovery
- •2.1 Introduction
- •2.1.1 Introduction to Drug Design and Discovery
- •2.1.2 Brief History of Small-Molecule Drug Discovery
- •2.1.3 Importance of Bioactive Small Molecules in Drug Discovery
- •2.2.1 Structure-Based Methods
- •2.2.2 Ligand-Based Methods
- •2.2.3 Network-Based Methods
- •2.3 Natural Products in Bioactive Small-Molecule Discovery
- •2.3.1 Plant Primary and Secondary Molecules as Bioactive Molecules
- •2.3.2 Anticancer Agents as Bioactive Molecules
- •2.3.3 Antiviral Agents as Bioactive Molecules
- •2.3.4 Antimalarial Agents as Bioactive Molecules
- •2.6.6 Toxicity and Side Effects
- •2.6.7 Cost-Effectiveness, Synthetic Feasibility, and Scalability
- •2.6.8 Structural Diversity and Novelty
- •2.6.9 Patentability and Intellectual Property
- •2.3.5 Marine Bioactive Products
- •2.4.1 Importance of DFT in Small-Molecule Drug Discovery
- •2.5 Application of DFT to Bioactive Small Molecules
- •2.5.1 HOMO–LUMO Calculation
- •2.5.1.1 Molecular Electrostatic Potential (MEP) Map
- •2.5.1.3 Natural Bond Orbital (NBO) Analysis
- •2.5.1.4 Implementations and Tools
- •2.6.1 Target Identification and Validation
- •2.6.2 Target Specificity
- •2.6.3 Bioavailability and Pharmacokinetics
- •2.6.4 Chemical Structure and Drug-likeness
- •2.6.5 Safety and Toxicity
- •2.7 Conclusion
- •References
- •3. Novel Drug Targets for Small Molecule-based Drug Discovery
- •3.1 Introduction
- •3.2 Drug Target Identification
- •3.3 Classification of Novel Drug Targets
- •3.3.1 Transcription Factors
- •3.3.2 Cytokines
- •3.3.3 Chaperones
- •3.3.4 Viral Targets
- •3.3.5 G Protein-coupled Receptors
- •3.3.6 Transporters
- •3.3.7 Enzymes
- •3.3.8 RNA Targets
- •3.4 Small Molecules as Drugs
- •3.5 Conclusion
- •References
- •4.1 Introduction
- •4.2 Structure-Based Drug Discovery Concept
- •4.2.1 Structure Generation of the Target
- •4.2.1.1 The Detailed Description of Each Tool
- •4.2.2 Active Binding Site Within the Target
- •4.2.2.1 The Detailed Description of Each Tool
- •4.2.2.2 Molecular Docking Analysis
- •4.2.2.3 The Detailed Description of Each Tool
- •4.2.3 Molecular Dynamic Simulations
- •4.2.3.1 The Detailed Description of Each Tool
- •4.3 Ligand-Based Drug Discovery Concept
- •4.3.1.1 The Detailed Description of Each Tool
- •4.4 Structure- and Ligand-Based Assisted Studies
- •4.4.1 The Detailed Description of Each Tool
- •4.4.2 The Detailed Description of Each Tool
- •4.5 Advancement and Challenges in SBDD and LBDD
- •4.6 Conclusion
- •References
- •5. Virtual Screening and Lead Discovery
- •5.1 Introduction to Virtual Screening and Lead Discovery
- •5.1.1 Overview of Drug Discovery Process
- •5.1.2 Role of Virtual Screening
- •5.1.3 Importance of Lead Discovery
- •5.2 Molecular Targets and Biomolecular Structures
- •5.3 Virtual Screening Approaches
- •5.3.1 Structure-based Virtual Screening
- •5.3.2 Ligand-based Virtual Screening
- •5.3.3 Hybrid Approaches
- •5.4 Databases and Compound Collections
- •5.4.1 Overview of Chemical Databases
- •5.4.2 Compound Filtering and Preparation
- •5.4.3 Diversity and Size of Compound Collections
- •5.5 Molecular Docking
- •5.5.1 Principles of Molecular Docking
- •5.5.2 Docking Algorithms and Scoring Functions
- •5.5.3 Validation of Docking Results
- •5.6 Pharmacophore Modeling
- •5.6.1 Concept of Pharmacophores
- •5.6.2 Generating Pharmacophore Models
- •5.6.3 Applications in Lead Discovery
- •5.7 Quantitative Structure–Activity Relationship (QSAR)
- •5.7.1 Basics of QSAR
- •5.7.2 Model Development and Validation
- •5.7.3 QSAR in Virtual Screening
- •5.8 Machine Learning and AI in Virtual Screening
- •5.8.1 Introduction to Machine Learning and AI
- •5.8.2 Feature Selection and Model Training
- •5.8.3 Applications in Virtual Screening
- •5.9 Hit-to-Lead Optimization
- •5.9.1 Prioritizing Hits from Virtual Screening
- •5.9.2 SAR Analysis and Iterative Design
- •5.9.2.1 SAR Analysis (Structure–Activity Relationship)
- •5.9.2.2 Iterative Design
- •5.9.3 ADME/Tox Considerations
- •5.9.3.1 ADME (Absorption, Distribution, Metabolism, Excretion)
- •5.9.3.2 Toxicity Considerations
- •5.10 Case Studies and Examples
- •5.10.1 Exploration Protocol for Mutant-targeted PI3K Inhibitors
- •5.11 Challenges and Future Directions
- •5.11.1 Limitations of Virtual Screening
- •5.11.2 Emerging Technologies and Trends
- •5.11.3 Integration with High-throughput Experimentation
- •5.12 Ethical and Regulatory Considerations
- •5.12.1 Intellectual Property and Patents
- •5.12.2 Ethical Use of Computational Tools
- •5.12.3 Regulatory Approval Process
- •5.13 Conclusion
- •5.13.1 Future Prospects in Virtual Screening and Lead Discovery
- •5.13.2 Summary of Key Points
- •References
- •6. ADMET and Physicochemical Assessments in Drug Design
- •6.1 ADMET
- •6.1.1 Absorption
- •6.1.1.1 Solubility and Dissolution
- •6.1.1.2 Lipophilicity
- •6.1.1.3 Permeability
- •6.1.2 Distribution
- •6.1.3 Metabolism
- •6.1.4 Excretion
- •6.1.5 Toxicity
- •6.2 Physicochemical Assessments
- •6.2.1 Partition Coefficient
- •6.2.2 Log D: Ionizable Compound Lipophilicity
- •6.2.2.1 Methods for Calculating Lipophilicity
- •6.2.2.2 Direct Experimental Determination of Lipophilicity
- •6.2.2.3 Indirect Experimental Determination of Lipophilicity
- •6.2.3 Acid–Base Properties and Ionization
- •6.2.4 Solubility
- •6.2.5 Polymorphism
- •6.2.6 Molecular Weight
- •6.2.7 Number of Hydrogen Bond Donors (HDB) and Acceptors (HDA)
- •References
- •7. In Silico Modeling and Drug Design
- •7.1 Introduction
- •7.2 Target Identification
- •7.2.1 Experimental Approaches
- •7.2.2 Computational Target Identification
- •7.2.3 Target Validation
- •7.3 Computer-Aided Drug Design
- •7.3.1 Ligand-based CADD
- •7.3.2 Structure-Based CADD
- •7.4 ADMET Assessment
- •7.5 Conclusion
- •References
- •8. Pharmacophore Modeling in Drug Design
- •8.1 Introduction
- •8.1.1 The Role of Pharmacophore Modeling in Drug Design
- •8.1.2 Historical Perspective and Evolution of Pharmacophore Concepts
- •8.2 Essential Concepts in Pharmacophore Hypothesis Generation
- •8.2.1.1 Partitioning Initial Data into Distinctive Datasets
- •8.3 Diverse Approaches to Pharmacophore Modeling
- •8.3.1 Ligand-Based Pharmacophore Modeling
- •8.3.2 Structure-Based Pharmacophore Modeling
- •8.4 Application of Pharmacophore Modeling
- •8.4.1 Applications of Pharmacophore-Based Virtual Screening
- •8.4.1.1 Drug Discovery
- •8.4.2 Applications in Drug Target Fishing
- •8.4.3 Applications in Ligand Profiling
- •8.4.4 Applications in Docking
- •8.4.5 Applications in ADMET
- •8.4.6 Modulation of the Immune System
- •8.5 Emerging Trends in Pharmacophore Model Development
- •8.5.1 Involvement of Machine Learning
- •8.5.2 Prediction of Pharmacokinetic Properties
- •8.5.3 Structural Biology and Protein Functionality Studies
- •8.5.4 Integration with MDs Simulations
- •8.6 Case Studies
- •8.6.1 Case 1
- •8.6.2 Case 2
- •8.7 Challenges in Pharmacophore Modeling
- •8.8 Conclusion
- •Acknowledgments
- •References
- •9. Scaffold Hopping and De Novo Drug Design
- •9.1 Introduction
- •9.2 Scaffold Hopping
- •9.2.1 Classification of Scaffold Hopping
- •9.2.1.1 1° Hop: Heterocycle Replacement
- •9.2.1.2 2° Hop: Ring Opening and Closure: Pseudo Ring Structures
- •9.2.1.3 3° Hop: Pseudopeptides and Peptidomimetics
- •9.2.1.4 4° Hop: Topology/Shape-Based Scaffold Hopping
- •9.2.2 Advantages of Scaffold Hopping
- •9.2.3 Disadvantages of Scaffold Hopping
- •9.2.4 Reasons for Scaffold Hopping
- •9.2.5 Properties and Key Methods of Scaffold Hopping
- •9.3 De Novo Drug Design
- •9.3.1 Classification of De Novo Drug Design
- •9.3.1.1 Structure-based Drug Design
- •9.3.1.2 Ligand-based Drug Design
- •9.3.1.3 De Novo Design Strategies
- •9.3.1.4 Artificial Intelligence (AI) and Machine Learning-based Design
- •9.3.1.5 Hybrid Approaches
- •9.3.2 Basic Principle of De Novo Drug Design
- •9.3.3 Application of De Novo Drug Design
- •9.3.4 Historical Overview of Scaffold Hoping and De Novo Drug Design
- •9.3.5 Methodological Approaches in De Novo Drug Design
- •9.3.5.1 Structure-based De Novo Drug Design
- •9.3.5.2 Ligand-based De Novo Drug Design
- •9.3.5.3 Generation of Drug-Like Molecular Fragments
- •9.3.5.4 Similarity Searching
- •9.3.5.5 Selection of Target Reference Structure
- •9.3.5.6 Similarity Analysis of De Novo-generated Compounds
- •9.3.5.7 Evaluation of Scaffold Diversity
- •9.4 Results and Discussion
- •9.4.1 Generation of Drug-Like Molecular Fragments
- •9.4.2 De Novo Design with a Single Reference Structure
- •9.4.3 De Novo Design with a Focused Set of Five Similar Templates
- •9.4.4 De Novo Design with a Diverse Set of Five Templates
- •9.6 Case Study
- •9.6.1 De Novo Drug Design
- •9.6.2 Scaffold Hopping
- •9.7 Conclusion
- •References
- •10. Fragment-based Drug Design and Drug Discovery
- •10.1 Introduction
- •10.2 The Process of Finding Fragments
- •10.3 FBDD Strategies
- •10.4 Case Studies
- •10.5 Conclusion and Future Perspectives
- •References
- •11. AI/ML Approaches in Drug Design
- •11.1 Introduction
- •11.2 Traditional Drug Design Methods
- •11.2.1 The Rise of Computational Methods
- •11.2.2 The Importance of AI/ML in Modern Drug Design
- •11.3 AI/ML Landscape in Drug Design
- •11.3.1 AI/ML Algorithms and Methods
- •11.3.1.1 Machine Learning Models
- •11.3.1.2 Neural Networks
- •11.3.2 Applications in Drug Design
- •11.3.2.1 Peptide Synthesis
- •11.3.2.2 Molecular Design
- •11.3.2.3 Virtual Screening (VS)
- •11.3.2.4 Quantitative Structure–Activity Relationship Models
- •11.3.2.5 Drug Repurposing
- •11.3.3 Challenges and Failures
- •11.4 Ethics, Reliability, and Regulatory Issues
- •11.5 Future Directions
- •11.6 Conclusion
- •References
- •12. Network-based Methods in Drug Discovery
- •12.1 Introduction
- •12.1.1 Background of Drug Discovery Future Challenges
- •12.1.2 Single Target Approach Limitations
- •12.1.3 Emergence of Network Biology and Polypharmacology
- •12.2 Network Pharmacology: Practical Guide
- •12.2.1 Common Network Pharmacology Databases
- •12.2.1.1 Network Pharmacology-Related Databases and Data Analysis Tools
- •12.2.1.2 Exploring IMPPAT Network Pharmacology Databases
- •12.2.1.3 Target Genes of Phytoconstituents
- •12.2.2 Network Analysis and Visualization
- •12.2.3 Applications of Network Pharmacology in Drug Discovery
- •12.3 Ayurveda and Traditional Indian Medicine
- •12.3.1 Overview of Ayurveda and Its Complex Formulations
- •12.3.2 Diversity of Ingredients and Bioactive Compounds in Ayurvedic Medicines
- •12.4 Network Pharmacology in Herbal Remedies
- •12.4.1 Application of Network Pharmacology in Herbal Drug Discovery
- •12.4.1.1 Cancer
- •12.4.1.2 Cardiovascular Diseases (CVDs)
- •12.4.1.3 Diabetes Mellitus (DM)
- •12.4.2 Screening Pharmacological Efficacy of Herbal Remedies
- •12.4.3 Utilizing Network Pharmacology to Understand Complex Diseases
- •12.5 Conclusion and Future Prospects
- •References
- •13. Rational Design of Natural Products for Drug Discovery
- •13.1 Introduction
- •13.2 Natural Products for the Development of New Drugs
- •13.3 Criteria for Selecting Natural Products for Drug Design
- •13.4 Importance of Biodiversity in Sourcing Natural Products
- •13.5 Structural Elucidation of Natural Products
- •13.6.3 High-Throughput Screening Methods for Efficient Compound Selection
- •13.6.4 Molecular Dynamics Simulations for Predicting Solubility and Stability
- •13.6.5 ADMET Attributes Predicted In Silico
- •13.7 Formulation Challenges with Natural Products
- •13.8 Quality by Design (QbD) Approaches
- •13.8.1 Use of Computational Models for Formulation Optimization
- •13.9 Conclusion
- •References
- •14. Design of Enzyme Inhibitors in Drug Discovery
- •14.1 Introduction
- •14.3 Classification of Enzyme Inhibitors
- •14.3.1 Reversible Inhibitors
- •14.3.2 Irreversible Inhibitors
- •14.3.3 Competitive Inhibitors
- •14.3.4 Noncompetitive Inhibitors
- •14.3.5 Allosteric Modulators
- •14.4.1 Structure-Based Design
- •14.4.2 Computer-Aided Design
- •14.4.3 Fragment-Based Design
- •14.4.4 Virtual Screening Method
- •14.4.4.1 Ligand Based
- •14.4.4.2 Receptor Based
- •14.4.5 Natural Product-Based Discovery
- •14.4.6 Using Iterative Protein Crystallographic Analysis
- •14.4.7 Utilization of Covalent Inhibitors
- •14.4.8 Encapsulation Techniques
- •14.4.9 Based on Active-Site Specificity
- •14.4.10 Machine Learning Inhibitor Design
- •14.4.11 Enzyme-Templated Dynamic Combinatorial Chemistry
- •14.5 Limitations and Challenges
- •14.6 Future Directions
- •14.7 Conclusion
- •References
- •15.1 Introduction
- •15.2 Peptides as Therapeutics
- •15.2.1 Peptide Antibiotics
- •15.2.1.1 Peptides in Bone Diseases
- •15.2.1.2 Peptides in Cancer
- •15.2.1.3 Peptides in Metabolic Diseases
- •15.2.1.4 Peptides in Gastrointestinal Diseases
- •15.2.2 Advantages and Limitations of Peptide Therapeutics
- •15.2.3 FDA-Approved Peptide Therapeutics
- •15.2.4 Peptide-Based Entities in Clinical Trials
- •15.2.5 Peptide Synthesis and Diversification
- •15.2.5.1 Chemical Synthesis of Peptides
- •15.2.5.2 Chemical Modification of Peptide and Peptidomimetics
- •15.2.5.3 Backbone Modification of Peptides
- •15.2.5.4 Side-Chain Modification of Peptides
- •15.2.5.5 Peptide Cyclization
- •15.2.5.6 Peptide Mimicking of α-Helices and Stabilization
- •15.2.5.7 Peptide Mimicking of β-Strands and β-Sheets
- •15.2.5.8 Peptide Production by Recombinant Technology
- •15.2.5.9 Peptides Modification by Genetic Code Expansion
- •15.2.5.10 PEGylation of Peptides and Proteins
- •15.3 New Technologies for Peptide-Based Drug Discovery
- •15.3.1 Phage Display
- •15.3.2 mRNA Display
- •15.3.3 DNA-Encoded Libraries
- •15.3.4 Cell-Penetrating Peptides
- •15.3.5 Macrocyclic Peptides
- •15.4 Computational Approaches in Peptide Drug Discovery
- •15.5 Conclusion
- •References
- •16. Rational Design of Drugs for Neurodegenerative Disorders
- •16.1 Introduction
- •16.2 Common Mechanism of Neurodegeneration
- •16.3 Brief Overview of Computational Methods in Drug Design
- •16.4 Parkinson’s Disease as Prevalent Neurodegenerative Disorder
- •16.4.1 Epidemiology of Parkinson’s Disease
- •16.4.2 Pathogenesis of PD
- •1) Accumulation of Lewy bodies in substantia nigra
- •2) Mitochondrial dysfunction
- •3) Genetic factors
- •4) Neuroinflammation
- •5) Impaired protein handling
- •6) Oxidative stress
- •7) Environmental toxins
- •16.4.3 Signaling Pathway of Parkinson’s Disease
- •1) DA signaling
- •2) MAPK/ERK pathway
- •3) PI3K/Akt/mTOR pathway
- •4) Wnt/β-catenin pathway
- •5) NF-κB (nuclear factor-κB) pathway
- •6) Autophagy-lysosomal pathway
- •7) JNK (c-Jun N-terminal kinase) pathway
- •8) AMPK (AMP-activated protein kinase) pathway
- •9) Nrf2 (nuclear factor erythroid 2-related factor 2) pathway
- •16.4.4 Enzymatic Targets in Parkinson’s Disease
- •1) MAO-B (monoamine oxidase B)
- •2) COMT (catechol-O-methyltransferase)
- •3) LRRK2
- •4) GCase (glucocerebrosidase)
- •5) PARP-1 [poly(ADP-ribose) polymerase-1]
- •6) PINK1
- •7) DJ-1 (Parkinson protein 7)
- •8) Nrf2
- •16.4.5 Current Therapeutic Approaches to Treat PD
- •1) Drugs to treat motor symptoms of PD
- •2) Drugs to treat non-motor symptoms of PD
- •3) Disease-modifying therapies to treat PD
- •16.4.6 Current Therapeutic Challenges to Treat Parkinson’s disease
- •1) Symptomatic relief only
- •2) Motor fluctuations and dyskinesias
- •3) Limited efficacy in nonmotor symptoms
- •4) Disease progression
- •5) Side effects
- •6) Limited treatment options for advanced PD
- •7) Individual variability
- •16.4.7 Unmet Needs in Parkinson’s Disease Therapeutics
- •16.4.8 Significance of Computational Approaches in Parkinson’s Disease
- •16.4.9 Use of Computational Tools in Identifying Biomarkers
- •16.4.10 Neuroprotective Strategies Through Computational Insights
- •16.4.10.1 Computational Models for Neuroprotection
- •1) Target identification and validation
- •2) Drug repurposing
- •3) Alpha-synuclein aggregation inhibitors
- •4) Deep learning in biomarker discovery
- •5) Personalized medicine
- •6) Drug-induced neuroprotection
- •7) Optimizing clinical trials
- •1) ML and AI-based diagnostics
- •2) Wearable technology integration
- •3) Multimodal data fusion
- •4) Predictive modeling of disease progression
- •5) Network analysis of brain connectivity
- •6) Personalized treatment optimization
- •7) Data sharing and collaboration platforms
- •16.5 Conclusion
- •References
- •17. Rational Design of Anti-inflammatory Therapeutics
- •17.1 Introduction
- •17.2 Navigating Inflammation and its Microenvironment
- •17.2.1 Inflammatory Cell Infiltration and Vascular Permeability
- •17.2.2 Acidosis
- •17.2.3 Increased Oxidative Stress in Tissues
- •17.3 The Demand for Advanced Anti-inflammatory Medications
- •17.5 Rational Design of Anti-inflammatory Agents
- •17.5.2 New Anti-inflammatory Agent with Indoyl-imidazole Hybrids
- •17.5.3 Rational Design of Novel Aminopiperidinyl Amide
- •17.5.4 Lipid Nanoparticles (LNPs) as Anti-inflammatory Agents
- •17.6 Conclusion and Future Perspectives
- •Authors’ Contribution
- •References
- •18.1 Introduction
- •18.2 Treatment
- •18.3 Antibacterial Resistance
- •18.3.1 Mutation
- •18.3.2 Horizontal Gene Transfer (HGT)
- •18.3.3 Enzymatic Modification or Degradation
- •18.3.4 Target Site Modification
- •18.3.5 Decreased Permeability
- •18.3.6 Efflux Pumps
- •18.3.7 Plasmids
- •18.3.8 Transposons
- •18.3.9 Gene Amplification
- •18.3.10 Formation of Biofilms
- •18.3.11 Modified Metabolic Pathways
- •18.3.12 Adaptive Evolution
- •18.4.1 Structure- Based Drug Design
- •18.4.2 Modification of Existing Antibiotics
- •18.4.3 Bioisosterism
- •18.4.4 Prodrug Strategies
- •18.4.5 Similar Bacterial Components Target
- •18.4.6 Combine or Combination Therapy
- •18.4.7 Drug Repurposing
- •18.4.8 Resistant Mechanism Blocking
- •18.4.9 Improving Drug Delivery by Nanotechnology
- •18.4.10 Phage Intervention
- •18.4.11 Host Targeting
- •18.4.12 CRISPR-Cas Technique
- •18.4.13 Peptides as Antibacterials
- •18.4.14 Immunizations and Immunotherapy
- •18.4.15 Natural Product Derivatives
- •18.4.16 Fragment- Based Drug Discovery (FBDD)
- •18.4.17 Metabolomics and Genetics
- •18.4.18 Cheminformatics
- •18.5 Summary and Conclusion
- •References
- •19. Rational Design of Antiviral Therapeutics
- •19.1 Introduction to Antiviral Therapeutics
- •19.1.1 Overview
- •19.1.2 Blueprints for Antiviral Drug Interventions
- •19.1.2.1 Protein Folding and Binding Sites
- •19.1.2.2 Conformational Changes
- •19.1.2.3 Protein–Protein Interactions (PPIs)
- •19.1.2.4 Capsid and Envelope Structures
- •19.1.2.5 Structural Vulnerabilities
- •19.1.2.6 Enzymatic Activities
- •19.1.2.7 Viral Attachment
- •19.1.2.8 Viral Assembly and Replication Machinery
- •19.1.2.9 The Host’s Immune Response
- •19.2 Targets for Antiviral Therapeutics and Inhibition Strategies
- •19.2.1 Enzyme Inhibitors
- •19.2.2 Antiviral Peptides
- •19.2.3 Antiviral Antibodies
- •19.2.4 Lipid-Mimicking Compounds
- •19.2.5 Vaccines
- •19.2.6 Immunomodulation
- •19.3 Rational Strategies for Antiviral Therapeutics
- •19.3.1 CADD and QSAR (Quantitative Structure–Activity Relationship)
- •19.3.2 AI and ML
- •19.3.3 Systems Biology and Network Pharmacology
- •19.3.4 CRISPR Systems
- •19.3.5 Nanotechnology-Based Design and Delivery Systems
- •19.3.6 Reverse Vaccinology
- •19.4 Conclusion
- •References
- •20. Rational Design of Anticancer Therapeutics
- •20.1 Introduction
- •20.2 Rational Design of Nanomedicine for Cancer Treatment
- •20.4.1 Particle Size
- •20.4.2 Shape
- •20.4.3 Surface Modification
- •20.6 Artificial Intelligence’s Progress in Anticancer Drug Development
- •20.6.1 Identification of Anticancer Drug Targets Using Artificial Intelligence
- •20.6.3 Artificial Intelligence-Based De Novo Anticancer Drug Design
- •20.6.4 Artificial Intelligence for Repurposing Anticancer Drugs
- •20.7 Conclusion
- •References
- •21. PROTAC and ProTide Strategies in Drug Design
- •21.1 Introduction
- •21.2 Drug Design: Past to Present
- •21.3 PROTAC Strategy in Drug Design
- •21.3.1 Ubiquitin Proteasome System and PROTACs
- •21.3.2 Chemical Formulations of PROTACs
- •21.3.3 Advent of PROTACs as Antiviral
- •21.3.4 NS3/4A-Targeting PROTACs Against HCV
- •21.3.4.1 Neuraminidase-Targeting PROTACs
- •21.4 Emergence of ProTide Technology in Drug Design
- •21.5 Approaches of ProTides in Drug Development
- •21.6 Implementation of ProTides as Nucleoside Analogs
- •21.6.1 Antiviral Applications of ProTides
- •21.7 Conclusion
- •References

113
protocol, employing ensemble docking to identify new selective agonists. RXR acts as a
heterodimeric partner for approximately one-third of the 48 human nuclear receptor superfamily
members, implying potential alterations in its ligand binding pocket upon interaction with different
heterodimerization partners. This heterodimerization significantly enhances DNA binding and
transcriptional activation, with reports indicating that increased expression of RXRα augments the
transcriptional response to ligand binding. Selective RXR agonists have demonstrated the ability to
enhance the antiproliferative and apoptotic responses of breast cancer cell lines to PPAR ligands.
Recent discoveries have unveiled RXR-selective ligands that not only inhibit the proliferation of
breast cancer cells resistant to all-trans RA in vitro but also induce regression of the disease in
animal models. Hence, RXR emerges as a promising therapeutic target for cancer treatment.
Considering the presence of multiple RXR receptor conformations due to binding with different
heterodimerization partners, our objective is to enhance the specificity of identified binders for a
given heterodimer partner by carefully selecting the RXR receptor structure for SBVS. Our method
entails selecting RXR conformations for SBVS based on four criteria:
● Conducting pairwise comparison of receptor conformations using RMSD calculations.
● Analyzing and clustering RXR structures based on binding-site shape and volume using SiteMap
(Figure 5.7).
● Docking a small database of known actives for a specific heterodimer partner to the resulting
shape-diverse subset of binding sites from steps (a) and (b) using Glide 5.8 SP and XP [73].
● Retrieving representative protein conformations for the structure of interest from MD simula-
tions using GROMACS [73].
Performing VS on three different subsets of RXR receptor conformations, arising from binding
to different heterodimerization partners selected as mentioned above, may increase the success
MD Simulations
conformer
generation
Binding site
prediction
Post-processing
Virtual
screening
Goal:
Discovery of
mutant specific inhibitors
for PI3Kα
Protocol evaluation
through in-vitro assays
10 compounds
4 actives
In vitro assaying
vdW filtering
pchem properties
clustering
Figure 5.6 Workflow for the discovery of mutant-specific PI3K inhibitors based on an SBVS protocol
involving conformer generation, binding site prediction, and compound post-processing.

114
rate of the process. Preprocessing for docking compound databases in this SBVS exercise involves
assigning protonation and tautomeric states as described previously. Compounds for assaying are
chosen based on the following criteria: Molecules that exhibit high scores when docked in the RXR
protein ensemble binding to the heterodimer partner of interest, while simultaneously displaying
low scores for RXR structures binding to heterodimer partners of no interest, are selected to
achieve selectivity. Subsequently, a post-processing step is applied to the top-scoring compounds
using ChemBioServer [74] and FAF-Drugs2 filtering tools [75] pharmacological property predic-
tion using the QikProp software. The workflow of this protocol is depicted in Figure 5.7.
5.11 Challenges and Future Directions
5.11.1 Limitations of Virtual Screening
VS is a computational technique used in drug discovery to identify potential drug candidates by
screening large chemical libraries, typically consisting of thousands to millions of compounds,
against a target of interest, such as a protein receptor implicated in a disease pathway. While VS has
become an integral part of the drug discovery process, it also comes with several limitations.
Scoring functions and accuracy: VS methods often rely on scoring functions to estimate the
binding affinity between a ligand and a target protein. However, these scoring functions may not
always accurately predict the binding affinity due to the complex and dynamic nature of
RMSD pairwise comparison
MD simulations
Binding site shape analysis
Docking of known agonists
Goal:
Protocol evaluation
through in-vitro
assays
Structural
ensemble selection
Ensemble
docking &
counterscreening
Compound
selection
Post-processing
Pharmacological
property
prediction
Discovery of
selective compounds
for
RXRa
Figure 5.7 Workflow for the discovery of selective RXR ligands based on an SBVS protocol of ED and
counter-screening.

115
protein–ligand interactions. A study by Gohlke et al. [16] highlights the challenges in accurately
predicting binding affinities, particularly for flexible binding sites and conformational changes
upon ligand binding.
Ligand flexibility: Conformational flexibility of ligands and proteins adds another layer of
complexity to VS. Traditional rigid docking approaches may fail to account for the conformational
changes required for binding, leading to false negatives or inaccurate predictions. Flexible docking
methods aim to address this issue by considering the flexibility of both ligands and receptors.
Library size and diversity: While VS allows for the rapid screening of large chemical libraries,
the quality and diversity of the compounds in these libraries greatly influence the success of the
screening process. Limited structural diversity within the chemical library can result in a biased
representation of chemical space and may overlook potential drug candidates. An analysis high-
lights the importance of chemical diversity in compound libraries for successful VS campaigns.
Computational resources and speed: VS methods often require significant computational
resources, especially when using computationally intensive techniques such as molecular dynam-
ics simulations or ensemble docking. Limited computational resources and time constraints may
restrict the thoroughness of the screening process or necessitate the use of simplified models,
potentially compromising accuracy. A study by Kitchen et al. [7] discusses the impact of computa-
tional resources on VS strategies.
Experimental validation and false positives: VS often generates a list of potential drug can-
didates that require experimental validation to confirm their biological activity and pharmacologi-
cal properties. False positives, where compounds exhibit activity in silico but fail in experimental
assays, can occur due to limitations in the scoring functions, incomplete representation of protein
flexibility, or neglect of relevant physicochemical properties. A study discusses the importance of
experimental validation in VS studies.
In conclusion, while VS is a valuable tool in drug discovery, researchers must be aware of its limi-
tations and continuously strive to improve methods and algorithms to overcome these challenges.
Addressing issues related to scoring accuracy, ligand flexibility, library diversity, computational
resources, and experimental validation will enhance the effectiveness of VS in identifying promis-
ing drug candidates.
5.11.2 Emerging Technologies and Trends
Emerging technologies like AI and ML are increasingly crucial in VS. Deep learning models, such
as CNNs, are gaining prominence for analyzing complex molecular structures. For example,
Alpha-Fold, a deep learning-based tool, has demonstrated remarkable accuracy in predicting pro-
tein structures. Integrating these technologies can significantly enhance the precision and effi-
ciency of VS.
5.11.3 Integration with High-throughput Experimentation
A promising trend is the integration of VS with high-throughput experimentation. In drug discov-
ery, VS can identify potential drug candidates quickly. These candidates are then subjected to high-
throughput experimental tests to validate their efficacy. For example, during the COVID-19
pandemic, VS identified existing drugs as potential treatments and high-throughput experiments
were used to rapidly confirm their effectiveness. This integration accelerates the drug discovery
process, especially in urgent situations like pandemics, where time is critical.

116
5.12 Ethical and Regulatory Considerations
5.12.1 Intellectual Property and Patents
Importance: Intellectual property (IP) and patents are critical in drug discovery. Companies
invest heavily in research, and IP protection incentivizes innovation by granting exclusive rights to
develop and market new drugs for a specified period.
Example: Consider a pharmaceutical company that discovers a novel compound through VS. To
protect their investment, they file a patent for the compound. This patent gives them the exclusive
right to develop and commercialize the drug for a certain number of years. IP protection encour-
ages pharmaceutical companies to invest in expensive drug development processes.
5.12.2 Ethical Use of Computational Tools
Responsible research: Ethical considerations are vital in using computational tools. Researchers
must ensure that their methods and data sources are ethical and accurate. Misuse of data or algo-
rithms can lead to erroneous results or unintended consequences.
Example: When using VS to identify potential drug candidates, it is essential to ensure that the
data sources are reliable and that the research is conducted with transparency and integrity.
Misrepresenting results or manipulating data unethically can have serious consequences.
5.12.3 RegulatoryApproval Process
Safety and efficacy: Regulatory approval is a crucial step before a drug can be marketed and pre-
scribed to patients. Regulatory agencies like the FDA in the United States evaluate a drug’s safety
and efficacy based on clinical trial data.
Example: A pharmaceutical company that has successfully identified a lead compound through
VS must conduct extensive preclinical and clinical trials to demonstrate its safety and effective-
ness. The regulatory approval process ensures that drugs reaching the market meet rigorous stand-
ards and do not pose undue risks to patients.
5.13 Conclusion
VS and lead discovery have indeed revolutionized the drug discovery process by offering efficient
and cost-effective methods for identifying potential drug candidates. The integration of computa-
tional techniques with experimental approaches has significantly accelerated the early stages of
drug development, allowing researchers to sift through vast chemical libraries and prioritize com-
pounds with higher chances of success. Moreover, advancements in technology, such as increased
computational power, improved algorithms, and enhanced molecular modeling tools, have further
bolstered the capabilities of VS methods.
5.13.1 Future Prospects in Virtual Screening and Lead Discovery
The integration of advanced ML and AI is anticipated to significantly enhance the accuracy and
predictive capabilities of VS models, consequently leading to more successful lead discoveries.
Furthermore, the integration of Big Data and Omics data, including genomics, proteomics, and

References 117
metabolomics, into VS approaches promises to provide a deeper understanding of drug–target
interactions. VS’s potential role in personalized medicine, tailoring drug treatments to individual
patients based on their genetic profiles, is expected to increase drug efficacy and minimize side
effects. Additionally, VS will continue to be instrumental in drug repurposing efforts, identifying
existing drugs for new therapeutic uses and potentially expediting the availability of treatments for
various diseases. The advancement of high-throughput computational screening methods will
enable faster and more efficient screening of larger compound libraries, thus broadening the scope
of lead discovery endeavors.
5.13.2 Summary of Key Points
In summary, VS and lead discovery involve using computational techniques to identify potential
drug candidates, optimizing them, and bringing them to market. Key points include:
● Virtual screening: The process of using computer simulations to identify compounds with
potential therapeutic activity.
● Lead discovery: The process of refining initial hits from VS into promising lead compounds.
● SAR analysis: Studying the relationship between the chemical structure of compounds and
their biological activity.
●
ADME/Tox considerations: Evaluating how compounds are absorbed, distributed,
metabolized, excreted, and assessing toxicity.
● Ethical and regulatory considerations: Ensuring ethical research practices and adhering to
regulatory standards in drug development.
● Future prospects: Advancements in AI, big data integration, and personalized medicine are
expected to shape the future of VS and lead discovery.
VS and lead discovery continue to drive innovation in drug development, offering hope for the
discovery of novel therapies for a wide range of diseases.
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