Caffeine
1,3,7-trimethyl-3,7-dihydro-1H-purine-2,6-dione
Overview
Caffeine belongs to Stimulants.
Effects
- Increased alertness and wakefulness, reduced fatigue and drowsiness, and improved reaction time, attention and concentration.
- A mild mood lift, and, especially at higher doses, jitteriness, anxiety, restlessness, tremor and insomnia.
- Peripheral effects: raised heart rate and blood pressure, increased gastric acid and (acutely) diuresis. Tolerance to several of these develops with regular use.
- Abrupt cessation after regular use causes withdrawal, headache, tiredness, irritability and difficulty concentrating, typically within 12–24 h.
Dosing & duration
Oral (beverages, foods, tablets). Consumed almost entirely orally in beverages, foods and tablets. Health authorities regard up to ~400 mg/day as low-risk for most adults and ~200 mg/day in pregnancy. Single moderate doses are ~40–200 mg. These are reference intakes, not a recommendation: sensitivity varies several-fold between people.
Dose ranges
Coffee ≈80–100 mg/cup · espresso ≈60–80 mg/shot · tea ≈30–50 mg · energy drink ≈80 mg · cola ≈35 mg
≤400 mg/day (adults), ≤200 mg/day in pregnancy
≈3–6 mg/kg (~200–400 mg) before exercise
Duration
≈15–45 min
Peak 30–120 min, effects ~3–5 h
Chemical & Physical Properties
| Formula | C8H10N4O2 |
| Molar mass | 194.19 g/mol |
| State | Solid |
| Melting point | 236.2 °C |
| Boiling point | 178 °C (sublimes) |
| Density | 1.23 g/cm³ at 18 °C (NTP, 1992) |
| Vapor pressure | 1×10⁻⁸ mmHg |
| pKa | 14 |
| LogP | -0.07 |
| Solubility | 10 to 50 mg/mL at 23 °C (NTP, 1992), 2.17 g/100mL, Solubility in water is increased by alkali benzoates, cinnamates, citrates or salicylates |
| Refractive index | Not reported |
Identifiers & Synonyms
| CAS | 58-08-2 |
| CAS (enantiomer) | |
| PubChem CID | 2519 |
| InChIKey | RYYVLZVUVIJVGH-UHFFFAOYSA-N |
| InChI | InChI=1S/C8H10N4O2/c1-10-4-9-6-5(10)7(13)12(3)8(14)11(6)2/h4H,1-3H3 |
| SMILES | CN1C=NC2=C1C(=O)N(C(=O)N2C)C |
Synonyms
- 1,3,7-Trimethylxanthine
- Guaranine
- Theine
- Caffeine
Pharmacodynamics & Biochemistry
Caffeine (1,3,7-trimethylxanthine) is the world's most widely used psychoactive drug. Its stimulant action comes almost entirely from non-selective antagonism of adenosine receptors. It blocks the A1, A2A, A2B and A3 subtypes, but at dietary intakes only A1 and A2A are meaningfully occupied (Ki ≈8–20 µM, matching the tens-of-µM plasma levels a few cups of coffee produce). Adenosine normally accumulates during waking and promotes sleep and sedation. By occupying its receptors caffeine releases that brake, raising arousal, alertness and neuronal firing. The alerting effect is driven largely by A2A blockade. A2A receptors sit in the sleep-promoting ventrolateral preoptic area and, in the striatum, form heteromers with dopamine D2 receptors. Antagonising them disinhibits downstream dopaminergic and histaminergic arousal circuits. This indirect enhancement of dopamine signalling, caffeine binds no dopamine receptor or transporter itself, underlies both the wakefulness and the mild reinforcing, habit-forming quality of caffeine. The textbook secondary actions: phosphodiesterase inhibition (raising cAMP) and ryanodine-receptor-mediated intracellular calcium release: are real but occur only at toxic, supraphysiological concentrations far above normal consumption. They contribute to overdose toxicity, not to the everyday cup-of-coffee effect. At dietary doses adenosine antagonism is essentially the whole story. Caffeine is metabolised in the liver by CYP1A2 to paraxanthine (~84%), theobromine and theophylline, which are themselves active. Regular use up-regulates adenosine receptors, producing tolerance to the alerting effect and a withdrawal syndrome (headache, fatigue, low mood) on abrupt cessation. CYP1A2 activity varies several-fold between people, induced by smoking, inhibited by drugs such as fluvoxamine, so both clearance and sensitivity differ widely.
Biological targets
- Adenosine A1
- Adenosine A2A
Binding & functional measurements
| Target | Measurement | Species |
|---|---|---|
| A2A receptor | pKi 5.1 | Human |
Pharmacokinetics
| Bioavailability | Oral ≈100% |
| Tmax | ≈30–60 min |
| Half-life | ≈3–5 h (prolonged in pregnancy and with CYP1A2 inhibitors) |
| Vd | Not reported |
| Protein binding | Not reported |
| Metabolism | Hepatic CYP1A2 to paraxanthine, theobromine, theophylline |
| Excretion | Renal (metabolites) |
Toxicology & Safety
Not reported
Caffeine is the most widely consumed psychoactive substance and is generally safe at dietary intakes. Health authorities put a low-risk ceiling around ≤400 mg/day for adults and ≤200 mg/day in pregnancy. Above that it causes 'caffeinism', anxiety, restlessness, insomnia, tremor, palpitations and diuresis, and can precipitate or worsen anxiety and cardiac arrhythmia. Acute overdose (roughly >1–2 g) brings vomiting, agitation, tachyarrhythmia, hypokalaemia and seizures. The estimated lethal dose is ~150–200 mg/kg (~10 g in an adult), but concentrated or pure caffeine powders and tablets have caused deaths from as little as a teaspoon, which prompted FDA action. A genuine, DSM-5-recognised dependence with withdrawal (headache, fatigue, irritability) develops even at ordinary intakes. Risk is higher in children, pregnancy, and people with impaired CYP1A2 metabolism or cardiac/anxiety disorders.[4][3][7]
Legal Status
US: Legal. Unregulated. UK: Legal. Unregulated. DE: Legal. Unregulated
Interactions & Contraindications
Drug interactions
Contraindications
No interactions or contraindications listed.
Usage & Context
- A dietary stimulant in coffee, tea, cola, energy drinks and chocolate, by far the most common use, taken for alertness and reduced fatigue.
- Therapeutic uses: apnoea of prematurity in neonates (caffeine citrate), an analgesic adjuvant (added to paracetamol, aspirin or ibuprofen), and an ergogenic aid for athletic performance.
- An over-the-counter alertness aid (tablets) and a common additive in weight-loss and 'pre-workout' supplements.
Sources & Evidence
- PubChem: Caffeine (CID 2519) — identifiers & computed properties
- FDA / DailyMed: Caffeine prescribing information — pharmacokinetics & metabolism
- Wikipedia: Caffeine (pharmacology, effects, toxicity, intake & legal status) CC BY-SA 4.0
- Fredholm BB, Bättig K, Holmén J, et al. (1999). Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 51:83-133.
PMID 10049999
- Nehlig A, Daval JL, Debry G (1992). Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev 17:139-70.
PMID 1356551 · doi:10.1016/0165-0173(92)90012-b
- IUPHAR/BPS Guide to PHARMACOLOGY: caffeine (ligand 407) — adenosine A1/A2A/A2B/A3 binding data CC BY-SA 4.0
- U.S. FDA: Pure and highly concentrated caffeine — safety & intake guidance
- Kull B, Arslan G, Nilsson C, et al. (1999). Differences in the order of potency for agonists but not antagonists at human and rat adenosine A2A receptors. Biochem Pharmacol 57:65-75.
PMID 9920286 · doi:10.1016/s0006-2952(98)00298-6
- Abo-Salem OM, Hayallah AM, Bilkei-Gorzo A, et al. (2004). Antinociceptive effects of novel A2B adenosine receptor antagonists. J Pharmacol Exp Ther 308:358-66.
PMID 14563788 · doi:10.1124/jpet.103.056036