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Pharmacology · Vol. 09

PHARMACOLOGY
/ How drugs find their targets

Small molecules and large biologics navigating a body of 1013 cells, looking for the one protein they were designed to bind.

A 13-slide field guide · Press → to begin
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Pharmacokinetics

ADME — what the body does to the drug

Every dose runs the same gauntlet. The fraction that reaches the target is often single digits.

A · ABSORPTION

Into the bloodstream

Oral, IV, transdermal, inhaled. Bioavailability varies wildly — insulin orally is ~0%.

D · DISTRIBUTION

Through tissues

Bound to plasma proteins, partitioned by lipophilicity. The blood-brain barrier turns most drugs away.

M · METABOLISM

Broken apart

The liver's CYP450 enzymes chop drugs into metabolites — sometimes activating, sometimes deactivating.

E · EXCRETION

Out

Kidneys (urine) and bile (feces) carry the remains. Half-life sets the dosing schedule.

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Pharmacodynamics

What the drug does to the body

Pharmacokinetics asks where the drug goes. Pharmacodynamics asks what happens when it gets there.

Almost every drug works by binding a protein — a receptor, an enzyme, an ion channel, a transporter — and changing what that protein does.

The relationship between concentration and effect is rarely linear. Doubling the dose rarely doubles the effect. Saturate the receptors and adding more accomplishes nothing… until you hit the toxicity ceiling.

log [DOSE] EFFECT EC₅₀
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Molecular Recognition

Receptors and ligands — keys and locks

RECEPTOR cell surface protein LIGAND drug molecule
  • AgonistActivates the receptor — mimics the natural ligand. Morphine on opioid receptors.
  • AntagnBlocks the receptor — occupies without activating. Beta-blockers, naloxone.
  • PartialActivates weakly even at full saturation — ceiling effect. Buprenorphine.
  • InverseReduces receptor activity below baseline — rare but real.
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Mechanism

Enzyme inhibitors — jamming the machinery

Many of the best-selling drugs in history work by sitting in an enzyme's active site so the substrate cannot.

HMG-CoA reductase

Statins

Block cholesterol synthesis in the liver. Atorvastatin, rosuvastatin. Among the most prescribed drugs on Earth.

Angiotensin-converting

ACE inhibitors

Lower blood pressure by stopping the conversion of angiotensin I → II. Lisinopril, enalapril.

Tyrosine kinase

Kinase inhibitors

Shut off rogue growth signals in cancer cells. Imatinib (Gleevec) turned chronic myeloid leukemia into a managed condition.

aspirin (acetylsalicylic acid) · C₉H₈O₄ HO O C O C O CH₃ irreversibly acetylates COX-1 and COX-2 → blocks prostaglandin synthesis → reduces pain, inflammation, clotting
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Therapeutic Classes

The drugs we actually take

vs. infection

Antibiotics

Penicillins, cephalosporins, macrolides, fluoroquinolones. Selectively kill bacterial machinery our cells lack.

vs. pain & inflammation

NSAIDs

Ibuprofen, naproxen, aspirin. Inhibit COX enzymes to reduce prostaglandins.

vs. severe pain

Opioids

Morphine, oxycodone, fentanyl. Bind μ-opioid receptors. Powerfully effective — powerfully addictive.

vs. depression

Antidepressants

SSRIs (sertraline, fluoxetine), SNRIs, MAOIs. Modulate serotonin / norepinephrine over weeks.

vs. clots

Anticoagulants

Warfarin, heparin, DOACs (apixaban, rivaroxaban). Prevent strokes, treat DVT — bleeding is the price.

others

Antihypertensives, antihistamines, antidiabetics…

Each class targets a different receptor, enzyme, or transporter. The categories keep multiplying.

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Dose — Response

The therapeutic window

DOSE → EFFECT TOXIC THERAPEUTIC SUB-THERAPEUTIC

Every drug has a dose where it works and a dose where it kills you. The ratio is the therapeutic index.

  • WidePenicillin, ibuprofen — forgiving margins, hard to overdose accidentally.
  • NarrowWarfarin, lithium, digoxin — therapeutic and toxic doses overlap. Blood monitoring required.
  • RazorChemotherapy — the toxic dose is the therapeutic dose. The art is killing tumor cells slightly faster than the patient.
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From Lab to Pharmacy

Drug development — 10–15 years, ~$2B

For every approved drug, roughly 10,000 starting molecules were screened. Most of the cost is paying for the failures.

YR 0–3
Discovery
Identify target. Screen libraries. Find a hit.
YR 3–6
Preclinical
Animal toxicology, pharmacokinetics, dosing.
YR 6–8
Phase I / II
Healthy volunteers (safety), then small patient cohorts (efficacy).
YR 8–12
Phase III
Thousands of patients. Randomized, controlled, blinded.
YR 12–15
FDA Approval
Review, label negotiation, post-market surveillance (Phase IV).

Phase III is where most candidates die — a drug that works in 200 people can fail in 2,000. The attrition rate from preclinical to approval is around 90%.

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Patent Cliff

Generics and biosimilars

A US drug patent runs 20 years from filing — effectively 8–12 years on market before competitors can copy.

When the patent expires, generic manufacturers must only prove bioequivalence: the active ingredient, the same blood concentration. They skip the discovery, the trials, the failures.

Prices typically fall 80–90% within a year. Atorvastatin went from $5/pill to under 10¢.

  • GenericIdentical small molecule. Same ibuprofen, different label. Bioequivalence study only.
  • BiosimFor biologics (antibodies, proteins) — can't be copied exactly. Must prove "no clinically meaningful difference."
  • BrandOften relaunches as authorized generic, or evergreens via reformulation, new indication, combination product.
  • Result~90% of US prescriptions are now generic. ~20% of spending.
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Side Effects

The price of doing pharmacological business

No drug is selective enough to bind only its intended target. Even when it is, the target does more than one thing.

Predictable

Dose-dependent

Stronger dose, stronger side effect. NSAIDs and ulcers, opioids and constipation, beta-blockers and fatigue.

Unpredictable

Idiosyncratic

Rare reactions specific to the patient — genetic variants, immune responses. Stevens-Johnson syndrome from carbamazepine.

Combinatorial

Drug-drug interactions

One drug induces or inhibits the CYP enzymes that metabolize another. Grapefruit juice does this too.

Adverse drug events cause an estimated ~100,000 US deaths annually — many from interactions in patients on 5+ medications. Polypharmacy is the silent epidemic of modern medicine.

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What's coming

The future of finding targets

precision

Targeted therapies

Drugs matched to a tumor's specific mutation, not its tissue of origin. Companion diagnostics required.

guided missiles

ADCs

Antibody-drug conjugates: an antibody finds the cancer cell, the linked toxin kills it. Trastuzumab deruxtecan.

code, not protein

mRNA

Deliver instructions, let the cell build the protein. COVID vaccines were the proof; cancer vaccines are next.

in silico

AI-designed molecules

Generative models propose binders for a protein structure. AlphaFold made every target druggable in principle.

Plus: gene therapies (CRISPR, AAV), PROTACs that destroy proteins instead of inhibiting them, gut-microbiome modulators, psychedelics in psychiatry. The pipeline has never been more diverse.

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The Honest Assessment

Most R&D fails. The survivors transform medicine.

Pharma is the only industry where 9 of every 10 products entering human trials never sell a single dose — and the model still works.

It works because the winners win enormously. Statins added years of life to entire populations. ART turned HIV from a death sentence into a chronic condition. Imatinib, GLP-1 agonists, hepatitis C cures, immunotherapy — each one rewrote a chapter of medicine.

The criticism is fair: prices are high, marketing is aggressive, the same molecule costs different amounts in different countries for opaque reasons. The replication crisis touches preclinical research too.

But the alternative — no industry willing to spend a decade and $2B on a 10% shot — is not better drugs. It is no new drugs.

A century ago, an infected cut could kill you. A bad heart meant the funeral home. Cancer meant months. The molecules in the bottle on your nightstand are the accumulated payoff of millions of failed experiments.

Pharmacology is humanity's best argument that biology is, in fact, engineerable.

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Closing

Further reading & viewing

Three centuries of trying to make molecules behave. Below, where to keep going.

REFERENCES

  • BOOKGoodman & Gilman, The Pharmacological Basis of Therapeutics
  • BOOKDruin Burch, Taking the Medicine: A Short History of Medicine's Beautiful Idea
  • BOOKBen Goldacre, Bad Pharma
  • PAPERDiMasi et al., "Innovation in the pharmaceutical industry" (J. Health Econ., 2016)
  • SITEDrugBank · PubChem · ClinicalTrials.gov

YOUTUBE

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