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Erythropoiesis-stimulating agents (ESAs) !

Recombinant erythropoietin and its long-acting analogues, which make the marrow produce red cells in the anaemia of kidney disease and chemotherapy.

Updated 2026-11-01

What they are

The kidney normally makes erythropoietin when oxygen delivery falls; in chronic kidney disease it does not, and anaemia follows. ESAs replace the hormone. They reduce transfusions but raise the risk of thrombosis, stroke and cardiovascular events when haemoglobin is pushed too high, so the lowest effective target is used.

Mechanism of action

They bind the erythropoietin receptor on erythroid progenitors in the marrow and, through JAK2–STAT signalling, keep them alive, dividing and maturing into red cells. Iron is needed for the response.

Target: Erythropoietin receptor (EPOR)

Drugs in this class

Others in the class

  • epoetin beta
  • epoetin theta
  • methoxy polyethylene glycol-epoetin beta
  • luspatercept (a different mechanism)

Test yourself

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

Why do patients with chronic kidney disease become anaemic?

The kidneys make too little erythropoietin.

What is the most common adverse effect of ESAs?

Hypertension.

Why is the haemoglobin not raised to normal?

It increases the risk of stroke, thrombosis and cardiovascular death.

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← All of pharmacology

Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.

Sources: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed., ch. 45 (McGraw Hill, 2023); Farmacología básica y clínica (Katzung), 16.ª ed., cap. 33 (McGraw Hill, 2025); Epoetin Alfa, Injection: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2019); eEML - Electronic Essential Medicines List (World Health Organization, 2025).

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Representative model, for educational purposes only.