Aspirin Chemical Structure

1. Identification

Summary
Aspirin (acetylsalicylic acid) is a nonsteroidal anti-inflammatory drug (NSAID) used for analgesia, antipyresis, anti-inflammation, and—at low doses—irreversible antiplatelet therapy for cardiovascular prevention.

Brand Names
Aspirin, Ecotrin, Aspro, Disprin, Bayer Aspirin (regional variants and generics)

Name
Aspirin (Acetylsalicylic acid)

Background
A salicylate ester developed in the late 19th century; its acetylation of platelet COX-1 underlies long-lasting antiplatelet effects. Widely available as IR/EC tablets, chewables, effervescents, and some combination products.

Modality
Small molecule

Groups
Approved; OTC/Rx (region-dependent)

Structure

Aspirin (acetylsalicylic acid) skeletal formula. Formula C₉H₈O₄; CAS 50-78-2.
Aspirin (acetylsalicylic acid) 2D chemical structure, C9H8O4, salicylate ester

Weight
~180.16 g/mol

Chemical Formula
C₉H₈O₄

Synonyms
Acetylsalicylic acid; 2-(acetyloxy)benzoic acid

External IDs
CAS: 50-78-2; PubChem CID: 2244; UNII: R16CO5Y76E; KEGG: D00109; ChEBI: 15365; ChEMBL: CHEMBL25


2. Pharmacology

Indication
Symptomatic treatment of mild–moderate pain and fever; adjunct for inflammatory conditions; low-dose antiplatelet use for secondary prevention of cardiovascular and cerebrovascular events (per guideline/label).

Associated Conditions
Headache, musculoskeletal pain, dysmenorrhoea, fever; chronic coronary disease, prior MI or ischemic stroke/TIA (antiplatelet use as indicated).

Associated Therapies
Often combined with P2Y₁₂ inhibitors in dual antiplatelet therapy (DAPT) when indicated; gastroprotection (e.g., PPI) in high GI-risk patients.

Contraindications & Blackbox Warnings
NSAID class warnings: GI bleeding/ulceration and CV risk (context-dependent). Contraindicated with aspirin/NSAID hypersensitivity, active bleeding, severe uncontrolled peptic ulcer. Reye’s syndrome risk: avoid in children/teens with viral illness. Caution in late pregnancy, bleeding disorders, and severe renal/hepatic impairment.

Pharmacodynamics
Analgesic/antipyretic/anti-inflammatory via prostaglandin reduction; antiplatelet via irreversible suppression of thromboxane A₂ in platelets (effect persists for platelet lifespan).

Mechanism of action
Irreversible acetylation of COX-1/COX-2 decreases prostaglandins and thromboxane. Platelets lack nuclei, so COX-1 activity is permanently reduced until new platelets are formed.

Absorption
Oral absorption is generally rapid; enteric coating or food can delay tₘₐₓ. Aspirin is quickly deacetylated to salicylic acid in plasma/tissues.

Volume of distribution
Approx. ~0.1–0.2 L/kg (salicylate), with pH-dependent tissue distribution.

Protein binding
High (~80–90% for salicylate), albumin-bound; binding decreases at higher concentrations.

Metabolism
Rapid ester hydrolysis to salicylate, followed by hepatic conjugation (salicyluric acid, salicyl phenolic/acyl glucuronides).

Route of elimination
Renal, largely as salicylate conjugates; urinary alkalinization enhances clearance (overdose management principle).

Half-life
Aspirin: short (≈15–20 min). Salicylate: ≈2–3 h at low doses, prolonged (non-linear) at high doses/overdose.

Clearance
Primarily renal for metabolites; rate increases with higher urinary pH.

Adverse Effects
Dyspepsia, nausea, epigastric pain; GI bleeding/ulcer, tinnitus (salicylism), bronchospasm in aspirin-sensitive asthma, rare severe skin reactions.

Toxicity
Overdose (salicylate poisoning) may cause tinnitus, hyperventilation, metabolic acidosis, hyperthermia, altered mental status; management includes activated charcoal (early) and urinary alkalinization/HD when indicated.

Pathways
COX-1/COX-2 acetylation; decreased TXA₂ (platelet) and PGE₂/PGI₂ (tissue).

Pharmacogenomic Effects/ADRs
No routine PGx testing; variability in clinical “aspirin resistance” often relates to adherence, drug interactions, or disease biology rather than a single genetic determinant.


3. Interactions

Drug Interactions

  • Anticoagulants/antiplatelets (e.g., warfarin, clopidogrel): ↑ bleeding risk—monitor.
  • Other NSAIDs (e.g., ibuprofen): may attenuate aspirin’s antiplatelet effect if taken near the same time; separate dosing per guidance.
  • SSRIs/SNRIs, corticosteroids, alcohol: additive GI bleeding risk.
  • Uricosurics (probenecid): low-dose aspirin may antagonize uricosuric effect.
  • Methotrexate: displacement/clearance effects may ↑ toxicity—use caution.

Food Interactions
Food and enteric coating can delay absorption; alcohol co-use increases GI toxicity risk.


4. Categories

ATC Codes
N02BA01 (analgesic/antipyretic) ; B01AC06 (antithrombotic)

Drug Categories
NSAID; Analgesic; Antipyretic; Antiplatelet; Small molecule

Chemical Taxonomy
Aromatic carboxylic acid ester; salicylate derivative

Affected organisms
Humans (therapeutic use)


5. Chemical Identifiers

UNII
R16CO5Y76E

CAS number
50-78-2

InChI Key
BSYNRYMUTXBXSQ-UHFFFAOYSA-N

InChI
InChI=1S/C9H8O4/c1-6(10)13-8-5-3-2-4-7(8)9(11)12/h2-5H,1H3,(H,11,12)

IUPAC Name
2-(acetyloxy)benzoic acid

SMILES
CC(=O)Oc1ccccc1C(=O)O


6. References

  • PubChem Compound Summary: Aspirin (CID 2244) — identifiers, formula, weight, canonical SMILES/InChI.
  • FDA/US labeling (DailyMed): Aspirin products — class warnings (GI/CV), pediatric Reye’s caution, dosing/administration.
  • StatPearls: Aspirin — pharmacology, PD/PK, toxicity, clinical cautions.
  • WHO Model List of Essential Medicines — aspirin listings and indications context.
  • ATC/DDD Index — N02BA01 and B01AC06 classifications, DDD.
  • NIST/InChI Trust resources — InChI and InChIKey confirmation.
  • Review guidance on ibuprofen–aspirin timing for antiplatelet effect preservation (regulatory safety communications and label Q&A).

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