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Biochemistry · Molecule

Thromboxane A₂ (TXA₂) !

TXA₂ is the platelet signal that calls more platelets and narrows vessels. Aspirin blocks its synthesis for the platelet's whole life.

Updated 2026-11-01

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Key facts

  • Made from PGH₂ by thromboxane synthase, mainly in platelets (COX-1).
  • It acts on TP receptors: platelet aggregation and vasoconstriction.
  • Its half-life is about 30 seconds; TXB₂ in serum or urine is measured instead.
Formula
C₂₀H₃₂O₅
PubChem
CID 5280497

Structure

  • A six-membered oxane ring with a strained four-membered oxetane bridge; it breaks down within seconds to inactive TXB₂.

Clinical notes

  • Low-dose aspirin prevents arterial thrombosis by blocking platelet TXA₂.
  • Excess TXA₂ relative to PGI₂ favours thrombosis, as with selective COX-2 inhibitors.
  • TBXAS1 deficiency causes Ghosal hematodiaphyseal dysplasia.

Pathways

Test yourself

Think of the answer, then tap the question to see it.

Which cell makes most thromboxane A₂, and with which COX?

The platelet, using COX-1.

What are the two main effects of TXA₂?

Platelet aggregation and vasoconstriction.

Why is TXB₂ measured instead of TXA₂?

TXA₂ breaks down within about 30 seconds to the stable, inactive TXB₂.

Add to my cards (3)

Molecules are shown in their neutral form, as the databases deposit them; in the cell the acids and phosphates are ionised.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: Thromboxane A2 (CID 5280497) (PubChem, NCBI, 2026) · Public domain; TBXAS1 gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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