Drugs & Medicines
Medicines and drugs are chemical substances that interact with biological molecules — enzymes, receptors, and ion channels — to produce a therapeutic effect. At the molecular level, a drug works by binding to a specific target protein, either activating it (agonist) or blocking it (antagonist). The shape and charge distribution of the drug molecule must be complementary to the active site of its target, a principle known as the lock-and-key model. Understanding the chemistry of common drug classes helps us appreciate how molecular structure directly determines biological function. The four major categories of everyday medicines are analgesics (pain relievers), antibiotics (bacterial infection fighters), antiseptics (surface antimicrobial agents), and antacids (stomach acid neutralisers). Each class operates through a distinct chemical mechanism. Analgesics like aspirin inhibit specific enzymes; antibiotics like penicillin disrupt bacterial cell wall synthesis; antiseptics like ethanol denature microbial proteins; and antacids like calcium carbonate undergo acid–base neutralisation reactions in the stomach. From a chemistry standpoint, drug design involves balancing several molecular properties: polarity (determining solubility and membrane permeability), functional groups (determining reactivity and binding affinity), and molecular size (determining absorption and distribution). This article examines real chemical structures, reaction equations, and mechanisms for each drug class, giving you the tools to analyse medicines from first principles rather than simply memorising facts.
- Analgesics — Aspirin (Acetylsalicylic Acid)
- Antibiotics — Penicillin and Its Mechanism
- Antiseptics — Ethanol, Phenol, and Hydrogen Peroxide
- Antacids — Neutralisation Chemistry
Analgesics — Aspirin (Acetylsalicylic Acid)
Aspirin (acetylsalicylic acid, C₉H₈O₄) relieves pain, fever, and inflammation by irreversibly inhibiting the enzyme cyclooxygenase (COX-1 and COX-2). COX enzymes catalyse the conversion of arachidonic acid into prostaglandins — lipid messengers that sensitise pain receptors and trigger fever. Aspirin contains an acetyl group (–OCOCH₃) attached to a salicylate ring. It transfers this acetyl group to a serine residue (Ser530) in the active site of COX, permanently blocking the enzyme's channel and stopping prostaglandin synthesis. This covalent modification is irreversible, which is why even a low daily dose (75 mg) has a prolonged antiplatelet effect lasting 7–10 days. Paracetamol (acetaminophen, C₈H₉NO₂) also inhibits COX but predominantly in the central nervous system; its exact mechanism involves the active metabolite AM404 and endocannabinoid pathways. Opioids such as morphine bind to μ-opioid G-protein-coupled receptors in the brain and spinal cord, hyperpolarising neurons and reducing pain signal transmission.
Antibiotics — Penicillin and Its Mechanism
Penicillin (core structure: 6-aminopenicillanic acid) contains a strained four-membered β-lactam ring fused to a thiazolidine ring. Bacteria build their cell walls from peptidoglycan, a polymer cross-linked by transpeptidase enzymes (penicillin-binding proteins, PBPs). The β-lactam ring of penicillin mimics the D-Ala–D-Ala terminal peptide sequence of the peptidoglycan precursor. When penicillin binds to the PBP active site, the strained β-lactam ring opens and forms a covalent acyl-enzyme intermediate, irreversibly inactivating the enzyme. Without functional transpeptidase, bacteria cannot reinforce their cell walls during growth; internal osmotic pressure causes the cell to lyse and die. Human cells lack peptidoglycan cell walls, so penicillin is highly selective and relatively non-toxic. Antibiotic resistance arises when bacteria produce β-lactamase enzymes that hydrolyse the β-lactam ring before it can reach PBPs. This is countered by co-administering β-lactamase inhibitors like clavulanic acid (e.g., Augmentin = amoxicillin + clavulanate).
Antiseptics — Ethanol, Phenol, and Hydrogen Peroxide
Antiseptics are applied to living tissue surfaces to kill or inhibit microorganisms. Ethanol (C₂H₅OH) at 70% v/v concentration is more effective than pure ethanol because water is needed to facilitate protein denaturation. Ethanol disrupts the hydrophobic core of proteins and dissolves the lipid bilayer of bacterial membranes. Phenol (C₆H₅OH, carbolic acid) — the first surgical antiseptic, used by Joseph Lister — denatures proteins through hydrogen bonding disruption and membrane permeabilisation at low concentrations, but is cytotoxic and has been replaced by safer derivatives like chlorhexidine. Hydrogen peroxide (H₂O₂) releases reactive oxygen species (·OH radicals) that oxidise and damage bacterial DNA, proteins, and lipid membranes. The decomposition reaction 2H₂O₂ → 2H₂O + O₂, catalysed by catalase enzyme in tissues, produces the characteristic fizzing seen on wounds. Iodine-based antiseptics (iodophors like povidone-iodine) release free iodine that rapidly iodinates tyrosine residues and oxidises thiol groups (–SH) in essential bacterial enzymes.
Antacids — Neutralisation Chemistry
The stomach maintains a pH of 1.5–3.5 using hydrochloric acid (HCl) secreted by parietal cells. Excess acid causes heartburn, gastritis, and peptic ulcers. Antacids are weak bases or carbonates that neutralise HCl through acid–base reactions. Common antacids include: (1) Sodium bicarbonate (NaHCO₃): NaHCO₃ + HCl → NaCl + H₂O + CO₂; rapid but produces CO₂ gas causing belching and systemic sodium loading. (2) Calcium carbonate (CaCO₃): CaCO₃ + 2HCl → CaCl₂ + H₂O + CO₂; releases CO₂ and provides supplementary calcium but may cause 'acid rebound'. (3) Magnesium hydroxide Mg(OH)₂ (milk of magnesia): Mg(OH)₂ + 2HCl → MgCl₂ + 2H₂O; no CO₂ produced; has a laxative effect at higher doses. (4) Aluminium hydroxide Al(OH)₃: Al(OH)₃ + 3HCl → AlCl₃ + 3H₂O; slower acting, causes constipation. Many modern products combine Mg(OH)₂ and Al(OH)₃ to balance laxative and constipating effects. Proton pump inhibitors (PPIs) like omeprazole are a more advanced treatment: they irreversibly inhibit the H⁺/K⁺-ATPase enzyme in parietal cells, blocking acid production at the source.
The Key Equation
- \ce{CaCO3} — Calcium carbonate (mol): The active ingredient in antacid tablets such as Tums; a weak base that neutralises stomach acid.
- \ce{HCl} — Hydrochloric acid (mol): Secreted by parietal cells in the stomach; responsible for the acidic gastric environment (pH 1.5–3.5).
- \ce{CaCl2} — Calcium chloride (mol): A soluble salt product that is safely absorbed into the bloodstream and excreted by the kidneys.
- \ce{CO2} — Carbon dioxide (mol): Gas released as a by-product; causes belching after taking carbonate-based antacids.
Worked Example
Problem. A patient takes an antacid tablet containing 500 mg of calcium carbonate (CaCO₃, M = 100 g/mol). Calculate the maximum mass of hydrochloric acid (M = 36.5 g/mol) that the tablet can neutralise, using the equation CaCO₃ + 2HCl → CaCl₂ + H₂O + CO₂.
Answer. One 500 mg calcium carbonate tablet can neutralise a maximum of 365 mg of hydrochloric acid.
Origins · 1 minAlexander Fleming and how this was discovered
Fleming discovered penicillin in 1928 when he noticed that the mould Penicillium notatum secreted a substance that lysed bacterial colonies on an agar plate. He identified that the active compound — which he named penicillin — selectively killed Gram-positive bacteria without harming human tissue. His observation launched the antibiotic era. Howard Florey and Ernst Chain later purified and mass-produced penicillin during World War II, saving millions of lives. Fleming, Florey, and Chain shared the 1945 Nobel Prize in Physiology or Medicine. Fleming almost discarded the contaminated petri dish that led to the discovery of penicillin — he showed it to a colleague on a whim before cleaning it, and that casual glance changed the history of medicine.
Related Concepts
- Acid–Base Reactions — Antacids work by neutralising stomach acid (HCl) through acid–base chemistry; understanding pH, neutralisation, and salt formation is essential to understanding how antacids work at the molecular level.
- Enzyme Inhibition — Aspirin and penicillin both act as irreversible enzyme inhibitors; understanding competitive vs. non-competitive and reversible vs. irreversible inhibition provides the mechanistic framework for how these drugs work.
- Functional Groups in Organic Chemistry — Drug activity is governed by specific functional groups — the β-lactam ring in penicillin, the acetyl ester in aspirin, the hydroxyl group in ethanol. Recognising these groups and their reactivity is foundational to pharmacological chemistry.
- Stoichiometry and Mole Calculations — Calculating effective doses of antacids, as demonstrated in the worked example, requires molar ratio calculations from balanced chemical equations — a core stoichiometry skill.