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+1. Drug Name
+
+    Adalimumab
+
+2. Mechanism of Action (MoA)
+
+    Adalimumab is a fully human monoclonal antibody (IgG1) that specifically binds to tumor necrosis factor-alpha (TNF-α), a pro-inflammatory cytokine. By neutralizing TNF-α, Adalimumab reduces inflammation and prevents immune-mediated tissue damage, making it effective in treating inflammatory bowel diseases such as Crohn’s disease (CD) and ulcerative colitis (UC).
+
+3. Pharmacokinetics
+
+    Absorption: Administered subcutaneously (SC), reaching peak plasma concentration in approximately 4–6 days.
+    Distribution: Exhibits a biphasic distribution with high specificity for TNF-α.
+    Metabolism: Degraded via proteolysis in the reticuloendothelial system.
+    Excretion: Eliminated mainly via intracellular catabolism, as monoclonal antibodies are not excreted through the liver or kidneys.
+
+4. ADME (Absorption, Distribution, Metabolism, Excretion)
+
+    Absorption: Bioavailability of approximately 64% after SC administration.
+    Distribution: Volume of distribution (Vd) is 4.7–6 L, with extensive binding to TNF-α.
+    Metabolism: Degraded into peptides and amino acids by proteolytic enzymes.
+    Excretion: Eliminated via reticuloendothelial and lymphatic systems, not through renal or hepatic pathways.
+
+5. Biodistribution
+
+    Primarily found in plasma and extracellular fluids, targeting inflamed intestinal tissue in IBD patients.
+    Crosses the placental barrier, but FcRn-mediated clearance reduces fetal exposure.
+    Minimal penetration into the central nervous system (CNS) due to its large molecular size.
+
+6. Target Binding
+
+    High specificity and affinity for TNF-α (~0.1 nM binding affinity).
+    Inhibits both soluble and transmembrane TNF-α, preventing its interaction with TNF receptors.
+    Reduces downstream pro-inflammatory signaling cascades, such as NF-κB and MAPK pathways.
+
+7. Pharmacodynamics
+
+    Reduces pro-inflammatory cytokine production, including IL-1, IL-6, and interferon-γ.
+    Decreases leukocyte migration and adhesion, preventing tissue damage in the gastrointestinal (GI) tract.
+    Improves mucosal healing, reducing disease severity in Crohn’s disease and ulcerative colitis.
+    Onset of action: Effects observed within 2–4 weeks, with sustained response in long-term therapy.
+
+8. Abbreviations
+
+    IBD – Inflammatory Bowel Disease
+    TNF-α – Tumor Necrosis Factor-alpha
+    SC – Subcutaneous
+    NF-κB – Nuclear Factor Kappa B
+    MAPK – Mitogen-Activated Protein Kinase
+    FcRn – Neonatal Fc Receptor
+    CD – Crohn’s Disease
+    UC – Ulcerative Colitis
+
+References
+
+    https://pubmed.ncbi.nlm.nih.gov/24831559/
+    https://www.cghjournal.org/article/S1542-3565%2813%2901050-1/fulltext
+    https://www.mdpi.com/2077-0383/12/22/7132
+