KU PPB 423 Lesson 7 B- Targeted antineoplastic drugs - Part 1
TARGETED ANTINEOPLASTIC DRUGS
Lesson 7B PPB 423 – Neoplastic Diseases & Anticancer Drugs
Instructor: Dr. Hilda Nderitu
Date: 23rd February 2022
INHIBITORS OF GROWTH FACTORS & RECEPTORS IN CANCER CELLS
Presentation Date: 12th February 2021
1. Introduction to Growth Factor Inhibitors
Target: Cancer cells
Drug Classes and Examples:
Epidermal Growth Factor Receptor (EGFR)
Function: EGFR inhibitors
Type: Small molecule protein tyrosine kinase inhibitors
Examples: Erlotinib, Gefitinib, Afatinib, Osimertinib
Antibody Inhibitors: Cetuximab, Panitumumab, Necitumumab
Human epidermal growth factor receptor 2 (HER2/Neu)
Type: HER2/Neu Inhibitors
Examples: Trastuzumab, Pertuzumab,
Small molecule inhibitors of EGFR & HER2 tyrosine kinases: Lapatinib, Neratinib
Platelet-Derived Growth Factor Receptor (PDGFR)
Type: PDGFR Inhibitors
Examples: Olaratumab
Hedgehog Pathway Inhibitors
Examples: Vismodegib, Sonidegib
2. Epidermal Growth Factor Receptor (EGFR) Inhibitors
Types of EGFR Inhibitors:
Small molecule protein tyrosine kinase inhibitors: Erlotinib, Gefitinib, Afatinib, Osimertinib
Antibody inhibitors: Cetuximab, Panitumumab, Necitumumab
3. Rationale for use of EGFR Inhibitors
Importance of EGFR:
Part of the Erb-B family (specifically ErbB1 or HER1).
Activated by ligands, essential for epithelial cell growth & differentiation.
Overexpression in various solid tumors, including:
Colorectal cancer
Head & neck cancer
Non-small cell lung cancer
Pancreatic cancer
4. Mechanism of Action of EGFR Inhibitors
EGFR Activation:
Ligand binding induces receptor dimerization leading to intracellular signaling activation.
Mutations enhance signaling for growth & survival advantage for cancer cells (e.g., T790M mutation).
5. Specific Drugs - Erlotinib
Mechanism of Action: Reversible inhibitor of EGFR, competitively inhibits ATP binding.
Pharmacokinetics:
Absorption: Bioavailability ~ 60%, peak plasma levels after 4 hours.
Metabolism: CYP3A4, CYP1A2, CYP1A1.
Elimination: Half-life ~36 hours, primarily hepatic clearance.
6. Clinical Indications for Erlotinib
Advanced or metastatic non-small cell lung cancer post platinum-based treatment failure.
Newly diagnosed non-small cell lung cancer with EGFR mutations.
Unresectable or metastatic pancreatic cancer (with gemcitabine).
7. Drug Interactions of Erlotinib
Avoid: grapefruit products, PPIs (reduce bioavailability).
Interactions with CYP3A4 inducers/inhibitors (e.g., warfarin – caution advised).
8. Adverse Effects of Erlotinib
Common: Rash, Diarrhea, Anorexia, Fatigue, Dyspnea, Nail disorders.
Serious: Severe rash, interstitial lung disease.
9. Other EGFR Inhibitors
Gefitinib:
Similar action as Erlotinib, indication for EGFR-mutated non-small cell lung cancer.
Adverse effects: Respiratory issues, skin reactions.
Afatinib:
Irreversible EGFR inhibitor, used for non-small cell lung cancer.
Adverse Effects: Diarrhea, skin rash, lung disease.
10. Resistance to EGFR TKIs
Resistance often arises from T790M mutation in EGFR, seen in ~60% of cases after prior treatments.
11. HER2/Neu Inhibitors
Mechanism and importance of HER2 in breast cancer.
Drugs: Trastuzumab, Lapatinib, Neratinib, Pertuzumab.
Rationale for use: Overexpression in 20-30% of breast cancers leads to aggressive tumors.
12. Summary of Adverse Effects
Trastuzumab: Cardiotoxicity, infusion reactions.
Lapatinib: Skin reactions, diarrhea.
Clinical monitoring required for cardiac effects.
13. Platelet-Derived Growth Factor Receptor Inhibitors
Inhibit PDGFR signaling, involve Olaratumab for treatment of sarcomas.
14. Hedgehog Pathway Inhibitors
Role in basal cell carcinoma and examples like Vismodegib and Sonidegib.
15. Tumor Angiogenesis Inhibitors
Overview of VEGF and angiogenesis in tumor growth.
Key drugs: Bevacizumab, Aflibercept.
Mechanism: Inhibit blood vessel formation to starve tumors.
16. Conclusion
Targeted therapies are vital in managing specific cancer types by blocking growth factors and their pathways.
Ongoing research and monitoring for resistance and adverse effects is crucial for optimizing cancer treatment.