What is ADME and why it matters

What is ADME?

ADME stands for Absorption, Distribution, Metabolism, and Excretion—essentially, the journey your medicine takes from the moment you take it until your body completely eliminates it. Think of it like a delivery system: the drug gets delivered (absorbed), transported to where it’s needed (distribution), modified so your body can get rid of it (metabolism), and finally removed (excretion).

Stage 1: Absorption (Drug Enters Body)

Drug moves from administration site into bloodstream. Key Points:Oral drugs absorbed in GI tract; takes time

First-pass metabolism: Liver breaks down oral drugs before they reach general circulation, reducing bioavailability.

Bioavailability (F): % of drug reaching bloodstream (IV = 100%, oral = 50-90%) Factors: Food, stomach pH, GI motility, drug chemistry

Stage 2: Distribution (Drug Spreads in Body)

Drug travels from blood to tissues and organs. Key Points:Volume of Distribution (Vd): How much of body the drug spreads into

Protein binding: Drugs stick to blood proteins (albumin); high binding = stays in blood longer Barriers: Blood-brain barrier blocks some drugs from reaching brain

Example: Warfarin 99% protein-bound → long half-life; Theophylline 40% bound → shorter half-life

Stage 3: Metabolism (Body Modifies Drug)

Liver transforms drug to make it eliminable.

Phase I: Cytochrome P450 (CYP) enzymes break apart or modify drug structure via oxidation, reduction, hydrolysis CYP3A4 handles ~75% of all drugs

Phase II: Conjugation adds water-soluble groups:Glucuronidation (morphine, acetaminophen)Sulfation (acetaminophen)Acetylation (isoniazid)Glutathione conjugation (detoxifies toxic metabolites) Factors affecting metabolism:Genetic polymorphisms (slow vs. fast metabolizers) Age, liver disease, concurrent drugs Enzyme inducers (rifampin, carbamazepine) speed metabolism

Enzyme inhibitors (ketoconazole, cimetidine) slow metabolism

Stage 4: Excretion (Drug Leaves Body)

Drug and metabolites removed via urine, bile, lungs.Key Points:Renal excretion (primary): Filtration, active secretion, reabsorption

Hepatic excretion: Larger metabolites eliminated in bile

Half-life (t₁/₂): Time for drug level to drop 50%Formula: t₁/₂ = 0.693 × (Vd / Clearance)Warfarin: 50 hours; Theophylline: 8 hours Kidney/liver disease → slower elimination → dose adjustment needed.

Why ADME Matters

Different routes, different doses: Oral needs higher dose due to first-pass metabolism.

Drug interactions: Drugs competing for metabolism or protein binding sites.

Kidney/liver disease: Must reduce doses; slower clearance.

Genetic differences: Some people are “fast” or “slow” metabolizers.

Elderly patients: Slower kidney/liver function = need lower doses.

Food/drug interactions: Grapefruit juice inhibits CYP3A4; charcoal grilling induces enzymes.

What your thoughts on ADME?

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Everyone who studies pharmacology comes across this topic but fails to understand its importance. The whole concept of pharmacodynamics is based on these principles. Formulating a drug according to the need is essential for its working principle.

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A drug’s ADME profile should be tailored based on the patient’s age, food intake, and metabolic disorders to maximize its efficiency.

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ADME studies helps in optimising correct dose and frequency for a drug.

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ADME forms the backbone of rational pharmacotherapy, this post explains it in a clinically relevant way.

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