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Erythropoietin is the glycoprotein hormone the kidneys release to tell bone marrow to make red cells; this product is the recombinant injectable version used to treat anaemia of chronic kidney disease, myelodysplasia and chemotherapy.
- Eschbach's 1987 phase I/II trial abolished transfusion dependence in dialysis patients and is the study that made recombinant erythropoietin a drug [1].
- The Normal Hematocrit Trial was stopped early because normalising haematocrit to 42% in haemodialysis patients with cardiac disease produced more deaths and non-fatal myocardial infarctions than a 30% target [2]; the first signal that more haemoglobin is not better.
- CHOIR (haemoglobin target 13.5 vs 11.3 g/dL, PMID 17108343) and CREATE [3] both failed to show benefit from normalising haemoglobin in non-dialysis CKD, and CHOIR found more composite cardiovascular events in the high-target arm.
- TREAT randomised 4,038 patients with type 2 diabetes, CKD and anaemia to darbepoetin alfa or placebo and found no reduction in death, cardiovascular events or end-stage renal disease, but a near-doubling of fatal or non-fatal stroke (5.0% vs 2.6%) [5].
- Bohlius's Lancet meta-analysis of 53 randomised trials with 13,933 cancer patients found ESAs increased on-study mortality (HR 1.17) and worsened overall survival (HR 1.06), the finding that defines the oncology boxed warning [6].
- Antibody-mediated pure red cell aplasia from neutralising anti-erythropoietin antibodies is a rare but severe complication that renders patients refractory to all ESAs.
Mechanism
The recombinant hormone is identical in sequence to the native one and acts on the same erythropoietin receptor on erythroid progenitors, rescuing them from apoptosis so more mature into red cells. Differences between the epoetin subtypes are in glycosylation, which changes half life rather than what the molecule does.
receptor fingerprint
EPOR (erythropoietin receptor) homodimer on erythroid progenitorsAgonist; induces the productive receptor dimer conformation
JAK2 (Janus kinase 2)Activated by EPOR dimerisation
STAT5A/STAT5B and BCL2L1 (Bcl-xL) inductionActivated downstream of JAK2
/ and RAS/MAPK pathwaysActivated downstream of EPOR
Hepcidin/iron availability axisFunctionally depleted by accelerated erythropoiesis
Safetyrisks and cautions, not medical advice
an injectable erythropoiesis stimulating agent; without haemoglobin, iron and blood pressure monitoring it drives haematocrit into a thrombotic range, and the class boxed warnings cover stroke, myocardial infarction and venous thromboembolism
Subjective profileweighing the evidence above
The tag that matters here is performance booster, because the people most likely to buy this hormone without a prescription are not anaemic. Pushing haematocrit up without haemoglobin, iron and blood pressure monitoring thickens blood into a thrombotic range, and the class carries boxed warnings for stroke, myocardial infarction and venous thromboembolism; the endurance sport scandals of the 1990s are what the unsupervised version looks like at scale. Anaemia of chronic kidney disease is a real indication managed with real monitoring, which is exactly why the page documents the hormone and declines the sourcing question.
Resources
No suppliers are provided for compounds like this. This entry is here for reference.
Research
- 1987first citedCorrection of the anemia of end-stage renal disease with recombinant human erythropoietin. Resu…
- 2009most recentRecombinant human erythropoiesis-stimulating agents and mortality in patients with cancer: a me…
- 1.Correction of the anemia of end-stage renal disease with recombinant human erythropoietin. Results of a combined phase I and II clinical trial
- 2.The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin
- 3.Normalization of hemoglobin level in patients with chronic kidney disease and anemia
- 4.Correction of anemia with epoetin alfa in chronic kidney disease
- 5.A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease
- 6.Recombinant human erythropoiesis-stimulating agents and mortality in patients with cancer: a meta-analysis of randomised trials
6 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
Notes and cautions
- Erythropoiesis-stimulating agents carry a BOXED WARNING for increased death, myocardial infarction, stroke, venous thromboembolism, thrombosis of vascular access, and tumour progression or recurrence.
- In chronic kidney disease the label directs clinicians to use the lowest dose sufficient to reduce the need for red-cell transfusion and warns that no trial has identified a haemoglobin target, dose or strategy that does not increase these risks; targets above 11 g/dL are specifically implicated [2][4][5].
- In cancer, ESAs shortened overall survival and increased tumour progression in breast, non-small-cell lung, head and neck, lymphoid and cervical cancers; they must not be used when the anticipated outcome is cure, must be started only when haemoglobin is below 10 g/dL with at least two additional months of chemotherapy planned, and must be stopped when that chemotherapy course ends.
- In the United States ESAs for oncology indications are governed by a risk-evaluation programme.
- Additional risks include hypertension and seizures, and pure red cell aplasia from neutralising antibodies, which requires permanent discontinuation of all ESAs.