Oxemia - Let freedom flow
How OXEMIA works

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.

Explore the clinical evidenceView prescribing information
Kidney releasing red blood cells into the bloodstream
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The normal oxygen-sensing response

  1. 1

    Low oxygen is sensed

    Oxygen gauge reading low

    When oxygen levels are low, cells signal that more oxygen is needed.

  2. 2

    HIF is stabilised

    Stabilised HIF protein

    HIF (hypoxia-inducible factor) escapes degradation and becomes active.

  3. 3

    Genes involved in EPO and iron handling are activated

    DNA double helix

    Active HIF turns on genes that increase EPO production and support iron availability.

  4. 4

    Erythropoiesis is supported

    Cluster of red blood cells

    More red blood cells are produced, improving oxygen delivery to tissues.

This is a natural response that helps the body adapt to low oxygen.

Mechanism of Action reference: Wang GL, Jiang BH, Rue EA, Semenza GL. Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O₂ tension. Proc Natl Acad Sci USA 1995; 92: 5510–5514.

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What changes in CKD

Impaired renal EPO production

Damaged kidneys produce less EPO, leading to lower stimulation of red blood cell production.

Chronic inflammation & 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.

Not every anaemia is caused by CKD. Many other conditions can cause low haemoglobin. Diagnosis and treatment decisions should be made by a clinician.

Source: DREAM-ND Phase III

Where desidustat acts

  1. 1

    PHD inhibition

    Desidustat inhibits PHD enzymes that normally break down HIF.

    PHD enzyme blocked by desidustat
  2. 2

    HIF stabilisation

    HIF accumulates and becomes active even at normal oxygen levels.

    Stabilised HIF protein
  3. 3

    Endogenous EPO production

    Active HIF increases EPO production by the kidneys.

    Endogenous erythropoietin molecules
  4. 4

    Improved iron metabolism

    HIF lowers hepcidin and increases genes that help iron absorption and mobilisation.

    Iron shield

Result: More iron available. More natural EPO. More red blood cell production.

HIF-1αHIF-1β(ARNT)HREHypoxia Response Elementp300/CBPNORMOXIAHYPOXIANormal OxygenLow OxygenO2HIF-1αCYTOSOLNUCLEAR

Biological outcomes

  • Angiogenesis
  • Invasion, Metastasis
  • Cancer Stemness
  • Metabolic Reprogramming

HIF-1 target genes

(VEGF, GLUT1, EPO…)

  • PHDProlyl Hydroxylase Domain
  • FIHFactor Inhibiting HIF
  • VHLVon Hippel–Lindau Protein
  • UbUbiquitin
  • p300/CBPCo-activators
  • HREHypoxia Response Element
Source: OXEMIA® (desidustat) Prescribing Information (PI)
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The haemoglobin and iron-utilisation story

Haemoglobin response demonstrated in Phase III studies

Non-dialysis CKD (DREAM-ND)

Significant improvement in haemoglobin vs darbepoetin over 24 weeks.

+1.95 g/dLvs baseline(Least square mean change)

Dialysis-dependent CKD (DREAM-D)

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)

DREAM-D

Hepcidin decreased from baseline; the difference vs epoetin alfa was not statistically significant.

−36.6 ng/mL(Mean change from baseline at Week 24)

China Phase III (Placebo-controlled)

Hepcidin levels decreased vs placebo by Week 9.

−32.7%(Mean % change)

Changes 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

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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
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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.

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Next steps