Low oxygen is sensed
When oxygen levels are low, cells signal that more oxygen is needed.
How OXEMIA worksWorking with the body’s
Working with the body’s
oxygen-sensing pathway
OXEMIA® (desidustat) is an oral HIF-prolyl hydroxylase domain inhibitor that stimulates erythropoiesis by increasing your body’s natural EPO production and improving iron utilisation.
Indicated for:
Anaemia in adult patients with chronic kidney disease (CKD)
on dialysis and not on dialysis.
The normal oxygen-sensing response
HIF is stabilised
HIF escapes degradation and becomes active.
Genes involved in EPO and iron handling are activated
Active HIF turns on genes that increase EPO production and support iron availability.
Erythropoiesis is supported
More red blood cells are produced, improving oxygen delivery to tissues.
iThis is a natural response that helps the body adapt to low oxygen.
What changes in CKD
Impaired renal EPO production
Damaged kidneys produce less EPO, leading to reduced stimulation of red blood cell production.
Chronic inflammation and higher hepcidin
Inflammation and reduced kidney clearance can raise hepcidin levels, limiting iron available for red blood cell production.
Iron may be present but less available
Iron stores may be normal or high, but less iron is mobilised and absorbed for effective use in erythropoiesis.
i
Source: DREAM-ND Phase III ↗Not every anaemia is caused by CKD. Many other conditions can cause low haemoglobin. Diagnosis and treatment decisions should be made by a clinician.
Where desidustat acts
PHD inhibition
Desidustat inhibits PHD enzymes that normally break down HIF.
HIF stabilisation
HIF accumulates and becomes active even at normal oxygen levels.
Endogenous EPO production
Active HIF increases EPO production by the kidneys.
Improved iron metabolism
HIF lowers hepcidin and increases genes that help iron absorption and mobilisation.
✓Result: More iron available. More natural EPO. More red blood cell production.
Source: OXEMIA® (desidustat) Prescribing Information (PI) ↗The haemoglobin and iron-utilisation story
Haemoglobin response demonstrated
in Phase III studies
Non-dialysis CKD (DREAM-ND)
(Least square mean change)
Significant improvement in haemoglobin vs darbepoetin over 24 weeks.
+1.95 g/dLvs baseline(Least square mean change)
Dialysis-dependent CKD (DREAM-D)
(Least square mean change)
Desidustat was non-inferior to epoetin alfa over 16–24 weeks.
+0.95 g/dLvs baseline(Least square mean change)
Hepcidin reductions observed
Supporting improved iron availability
DREAM-ND
Hepcidin levels decreased significantly vs darbepoetin by Week 9.
−37.2%(Mean % change)China Phase III (Placebo-controlled)
Hepcidin levels decreased vs placebo by Week 9.
−32.7%(Mean % change)iChanges in biomarkers such as hepcidin support the mechanism but should not be assumed to automatically translate into improved long-term clinical outcomes. Important outcome gaps remain.Review the systematic evidence →
From mechanism to evidence
Non-dialysis CKD
Phase III evidence (DREAM-ND)Desidustat demonstrated non-inferiority to darbepoetin for haemoglobin improvement over 24 weeks.
Explore non-dialysis evidence →Dialysis-dependent CKD
Phase III evidence (DREAM-D)Desidustat demonstrated non-inferiority to epoetin alfa for haemoglobin improvement over 16–24 weeks.
Explore dialysis evidence →Fair balance and limitations
Mechanism ≠ clinical outcomes
Mechanistic and biomarker effects do not automatically prove benefits on all clinical outcomes.
Different molecules, different evidence
HIF-PHI molecules should not be assumed to be interchangeable. Evidence must be evaluated molecule by molecule.
Certainty matters
The systematic review highlights important evidence gaps for some outcomes in non-dialysis CKD.
Always review safety information
See the approved indication, dosage, contraindications, warnings and precautions in the prescribing information.
Next steps
For patients & caregivers
Prepare for an informed conversation with your doctor.
Download questions to ask at your next appointment ↓
