Abstract
Desidustat (Oxemia™) is an orally bioavailable, small molecule, hypoxia-inducible factor-prolyl hydroxylase (HIF-PH) inhibitor developed by Zydus Cadila for the treatment of anaemia associated with chronic kidney disease (CKD), COVID-2019 infections and chemotherapy induced anaemia. Desidustat inhibits prolyl hydroxylase domain enzymes, resulting in the stabilisation of hypoxia-inducible factor which stimulates erythropoietin production and erythropoiesis. In March 2022, desidustat received its first approval in India for the treatment of anaemia in adults with CKD who are either on dialysis or not on dialysis. Desidustat is in clinical development in China for the treatment of anaemia in patients with CKD, in Mexico for the management of COVID-2019 infections and in the USA for the treatment of chemotherapy induced anaemia. This article summarizes the milestones in the development of desidustat leading to this first approval for anaemia associated with CKD.
Similar content being viewed by others
Digital Features for this AdisInsight Report can be found at https://doi.org/10.6084/m9.figshare.20128484 |
An orally bioavailable, small molecule, HIF-PH inhibitor is being developed by Zydus Cadila for the treatment of anaemia associated with CKD, COVID-2019 infections and chemotherapy induced anaemia |
Received its first approval on 7 March 2022 in India |
Approved for the treatment of anaemia in adults with CKD who are either on dialysis or not on dialysis |
1 Introduction
Renal anaemia is a common complication of chronic kidney disease (CKD), resulting from low erythropoietin (EPO) production by the failing kidney and immune activation [1, 2]. Hypoxia-inducible factors (HIF-1α, HIF-2α and HIF-3α) are heterodimeric transcription factors that regulate cellular response to hypoxia by altering gene expression in certain cell types [3, 4]. HIF-2α plays a key role in regulating erythropoiesis and iron metabolism [1, 3]. Under normal oxygen conditions, HIF-α subunits are targeted for hydroxylation by prolyl-hydroxylase domain enzymes (PHD1, PHD2, and PHD3) and then degraded, thereby inhibiting downstream signalling [1,2,3]. However, under hypoxic conditions, PHD-mediated hydroxylation of HIF-α is inhibited, resulting in the accumulation of HIF-α. HIF-α is them translocated to the nucleus where it heterodimerizes with HIF-β, resulting in the induction of hypoxia-responsive genes and ultimately stimulating production of endogenous EPO, improving iron metabolism and promoting erythropoiesis [1,2,3]. Given its central role in the hypoxic regulation of erythropoiesis, the HIF-PHD pathway is an attractive therapeutic target for the treatment of anaemia.
Desidustat (Oxemia™) is an orally bioavailable, small molecule, HIF-prolyl hydroxylase (HIF-PH) inhibitor developed by Zydus Cadila, for the treatment of anaemia associated with CKD, COVID-2019 infections and chemotherapy induced anaemia.
Desidustat inhibits PHD, resulting in the stabilisation of HIF which stimulates erythropoietin production and erythropoiesis. On 7 March 2022 [5], desidustat received its first approval in India for anaemia associated with CKD in patients either on dialysis or not on dialysis [6]. The recommended starting dosage in dialysis-dependent patients is desidustat 100 mg administered orally three times weekly [6]. In patients not on dialysis and untreated with an erythrocyte stimulating agent (ESA) agent, the recommended starting dosage is desidustat 100 mg three times weekly, and in patients switching from an ESA the recommended dosage is desidustat 100, 125 or 150 mg three times weekly, depending on the previous dose of epoetin, darbepoetin or methoxy polyethylene glycol-epoetin beta. Thereafter, desidustat dosage should be adjusted based on haemoglobin levels assessed every 4 weeks, with a maximum dosage of 150 mg three times weekly [6]. Desidustat is in clinical development in China for the treatment of anaemia in patients with CKD, in Mexico for the management of COVID-2019 infections and in the USA for the treatment of chemotherapy induced anaemia. Clinical development of desidustat has been discontinued in Australia.
1.1 Company Agreements
In January 2020, Zydus entered into a licensing agreement with China Medical System Holdings Limited (CMS) for the development and commercialization of desidustat in Greater China (Mainland China, Hong Kong Special Administrative Region, Macao Special Administrative Region and Taiwan) [7].
2 Scientific Summary
2.1 Pharmacodynamics
In preclinical studies, desidustat significantly and dose-dependently increased plasma EPO and reticulocyte counts, increased liver HIF-1α levels, decreased liver hepcidin levels and increased serum iron levels in normal and/or nephrectomized rats [8]. Desidustat also increased haemoglobin, haematocrit and red blood cell (RBC) counts in a chemotherapy (cisplatin)-induced anaemia mouse model [8]. Rodent models of acute and chronic renal failure suggested that the pharmacokinetics of desidustat are unlikely to be altered in CKD patients [9]. Desidustat reversed inflammation-induced anaemia in rodent models, as indicated by increased EPO, haemoglobin, haematocrit and iron levels, increased reticulocyte and RBC counts and decreased hepcidin levels [10].
In healthy volunteers receiving single-dose desidustat 10–300 mg, desidustat doses of 100–300 mg more consistently increased haemoglobin by > 0.5 g% and increased mean EPO levels in a dose-dependent manner [11]. The mean time to peak serum levels of EPO ranged from 10 to 72 h, with mean serum EPO returning to baseline levels within 24 h. Desidustat multiple doses of 100–300 mg also increased serum EPO, with peak levels reached 6–8 h after peak desidustat concentration is reached (tmax). In individuals receiving multiple dose desidustat 100–300 mg or placebo on days 1, 3 and 5, a dose-dependent increased in serum EPO was observed with desidustat 200 and 300 mg, and more desidustat than placebo recipients had haemoglobin increases of > 0.1% g and > 0.5% g at any timepoint. There was no apparent change in mean haematocrit, haemoglobin, and reticulocyte counts over time or between treatments in individuals receiving single or multiple doses of desidustat versus placebo [11].
Desidustat 100–200 mg increased EPO levels and decreased hepcidin and low-density lipoprotein cholesterol (LDL-C) levels versus placebo in a phase 2 study in pre-dialysis patients with CKD (CTRI/2017/05/008534) [12]. In the phase 3 DREAM-ND study (NCT04012957; Sect. 2.3.1.2) in non-dialysis-dependent patients with CKD, hepcidin levels reduced from baseline to greater extent with desidustat than with darbepoetin alfa at weeks 12 (p = 0.0032) and 24 (p = 0.0016) [13]. LDL-C levels were also significantly lower with desidustat than with darbepoetin alfa at week 24 (p = 0.0269), but no significant between-group differences were seen for the changes from baseline in high-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, total cholesterol, triglycerides and alipoprotein levels [13]. In the phase 3 DREAM-D study (NCT04215120; Sect. 2.3.1.1) in dialysis-dependent patients with CKD, there was no significant difference between desidustat and epoetin alfa recipients for the decrease from baseline in hepcidin levels at weeks 12 and 24 [14]. The decrease from baseline in total cholesterol and LDL-C at week 12 and alipoprotein at week 24 was greater with desidustat than with epoetin alfa (all p < 0.01) [14].
2.2 Pharmacokinetics
The pharmacokinetics of oral desidustat have been assessed in healthy volunteers [6], pre-dialysis CKD patients [6, 12] and dialysis-dependent CKD patients [6]. In healthy volunteers, peak plasma concentration (Cmax) of desidustat is reached in ≈ 1.3 h after a single oral dose of desidustat 50 mg under fasting condition [6]. Food delayed desidustat tmax and reduced desidustat exposure [Cmax and area under the concentration-time curve from time 0 to t (AUCt)] [6].
In patients with dialysis-dependent CKD who received single-dose desidustat 50, 100 or 150 mg within 2 h of dialysis (n = 8/dose), tmax is reached ≈ 2.5 h after dosing [6]. In pre-dialysis CKD patients, desidustat exposure (Cmax and AUCt) increased in a dose-dependent manner after single and multiple doses following treatment with desidustat 100, 150 or 200 mg (n = 11/dose) on alternate days for 6 weeks in a phase 2 study (CTRI/2017/05/008534) [6, 12]. No accumulation of desidustat was observed after multiple-dose administration (accumulation index ≈ 1) [6, 12]. Desidustat is highly (≈ 99%) plasma protein bound and is not preferentially distributed in erythrocytes [6].
In vitro desidustat was metabolically stable when incubated with human liver microsomes, human hepatocytes or recombinant human CYP isoforms. In pre-dialysis patients, desidustat was metabolized into two minor metabolites, hydroxylated and hydroxyl-glucuronide metabolites [6, 12]. Desidustat does not form reactive glutathione-protein adducts [6]. After a single oral dose of desidustat 10–300 mg in healthy volunteers in fasting condition, 27–41% of desidustat was excreted as unchanged drug in the urine; the hydroxylated and hydroxyl-glucuronide metabolites were also detected in the urine. The mean elimination half-life of desidustat was 6–15 h after a single 50–150 mg dose in dialysis-dependent CKD patients and 6–14 h after multiple-dose desidustat 100–200 mg on alternate days for 6 weeks in pre-dialysis CKD patients [6].
At therapeutically relevant concentrations, desidustat has minimal potential to cause CYP-mediated drug-drug interactions [6]. In in vitro studies, desidustat did not significantly inhibit CYP enzymes 1A2, 2C8, 2C9, 2C19, 2D6 and 3A4/5 half maximal inhibitory concentrations > 300 µM) and was not a time dependent inhibitor of CYP3A4/5. Desidustat 100 µM was not an inducer of CYP1A2 or CYP3A4 [6].
Features and properties of desidustat
Alternative names | Oxemia™; ZYAN-1; ZYAN-1-1001 |
Class | Acetic acids; amides; anti-anaemics; cyclopropanes; quinolines; small molecules |
Mechanism of action | Inhibits HIF-PH resulting in the stabilisation of HIF which stimulates EPO production and erythropoiesis |
Route of administration | Oral |
Pharmacodynamics | Decreased hepcidin, increased EPO, serum iron, haematocrit and haemoglobin levels, and increased reticulocytes and RBCs in normal/nephrectomized rats and/or rodent models of chemotherapy-or inflammation-induced anaemia |
Increased haemoglobin and EPO levels in healthy volunteers | |
Decreased hepcidin levels to a greater extent than darbepoetin alfa in patients with non-dialysis-dependent CKD | |
Decreased hepcidin levels to a similar extent as epoetin alfa in patients with dialysis-dependent CKD | |
Pharmacokinetics | Time to peak plasma concentration 2.5 h after single 50–150 mg dose in dialysis-dependent patients |
No accumulation after multiple dose administration | |
Mean elimination half-life 6–15 h after single 50–150 mg dose in dialysis-dependent CKD patients and 6–14 h after multiple doses of 100–200 mg on alternate days for 6 weeks in pre-dialysis CKD patients | |
Adverse events | |
Most frequent | Pyrexia, vomiting, asthenia, peripheral oedema |
ATC codes | |
WHO ATC code | B03X-A (other antianemic preparations); J05A-X (other antivirals) |
EphMRA ATC code | B3X (other anti-anaemic products, including folic acid, folinic acid); J5B9 (antivirals, others) |
Chemical name | 2-[[1-(cyclopropylmethoxy)-4-hydroxy-2-oxoquinoline-3-carbonyl]amino]acetic acid |
2.3 Therapeutic Trials
2.3.1 Anaemia in CKD
Phase 3 DREAM-D Study Oral desidustat was noninferior to subcutaneous biosimilar epoetin alpha in the treatment of anaemia (haemoglobin 8.0–11.0 g/dL) in patients with CKD (stage 5) on dialysis (≥ 2 times a week for ≥ 12 weeks) who were participating in the 24-week, randomized, open-label, multicentre, phase 3 DREAM-D study (NCT04215120) [14]. Patients (both ESA users and nonusers; mean age ≈ 51 years) were randomized to receive desidustat (n = 196) or epoetin alfa (n = 196) three times weekly for 24 weeks. The initial dose of desidustat was 100 mg in ESA-naïve patients and 100, 125 or 150 mg in ESA-experienced patients (based on prior ESA dose); epoetin alfa was administered at a dose of 50 IU/kg. Dosage adjustments were permitted during weeks 4–20 based on haemoglobin levels; iron supplementation was permitted to maintain adequate iron status. Mean haemoglobin level at baseline was 9.61 g/dL in the desidustat group and 9.55 g/dL in the epoetin alfa group. In the modified intent-to-treat population (mITT), the least-squares mean change in haemoglobin from baseline to weeks 16–24 (primary endpoint) in patients receiving desidustat (n = 184) was noninferior to that in patients receiving epoetin alfa (n = 189) [0.95 vs 0.80 g/dL], as the lower limit of the two-sided 95% confidence interval for the between-group difference was greater than the pre-specified noninferiority margin of − 1.0 g/dL (0.14 g/dL; 95% CI − 0.13 to 0.42). The proportion of haemoglobin responders was significantly higher in the desidustat group than in the epoetin alfa group (59.2% vs 48.4%; p = 0.038), where response was defined as achievement of target haemoglobin of 10–12 g/dL (average of weeks 16, 20 and 24) and posttreatment increase of ≥ 1 g/dL in haemoglobin by week 24. The median time to achieve target haemoglobin was significantly less in patients receiving desidustat than in patients receiving epoetin alfa (4 vs 8 weeks; p = 0.042) [14].
Phase 3 DREAM-ND Study Oral desidustat was noninferior to subcutaneous biosimilar darbepoetin alfa in the treatment of anaemia (haemoglobin 7.0–10 g/dL) in non-dialysis-dependent patients with CKD (stages 3–5) who were participating in the 24-week, randomized, open-label, multicentre, phase 3 DREAM-ND study (NCT04012957) [13]. Patients (mean age ≈ 53 years) were randomized to receive initial doses of desidustat 100 mg three times weekly (n = 294) or darbepoetin alfa 0.75 µg/kg (n = 294) for 24 weeks; dosage adjustments were permitted during weeks 4–20 based on haemoglobin levels. Iron supplement was given based on serum ferritin and transferrin saturation levels. Mean haemoglobin level at baseline was 8.99 g/dL in the desidustat and darbepoetin alfa groups. In the mITT population, the least-squares mean change in haemoglobin from baseline to weeks 16–24 (primary endpoint) in patients receiving desidustat (n = 268) was noninferior to that in patients receiving darbepoetin alfa (n = 261) [1.95 vs 1.83 g/dL], as the lower limit of the two-sided 95% confidence interval for the between-group difference was greater than the pre-specified noninferiority margin of − 0.75 g/dL (0.11 g/dL; 95% CI − 0.12 to 0.35). The proportion of haemoglobin responders was significantly higher in the desidustat group than in the darbepoetin alfa group (77.8% vs 68.5%; p = 0.018), where response was defined as achievement of target haemoglobin of 10–12 g/dL (average of weeks 16, 20 and 24) and posttreatment increase of ≥ 1 g/dL in haemoglobin by week 24. The median time to achieve target haemoglobin was similar in patients receiving desidustat and those receiving darbepoetin alfa (4 weeks in both groups) [13].
2.3.2 Phase 2 Study
Desidustat dose-dependently increased haemoglobin levels in patients with anaemia due to non-dialysis-dependent CKD who were participating in a 6-week, randomized, double-blind, placebo-controlled, phase 2, dose-ranging study (n = 117; CTRI/2017/05/008534) [12]. Patients (mean age ≈ 48 years) were randomized to receive desidustat 100, 150 or 200 mg or placebo on alternate days for 6 weeks in fasting conditions (n = 29–30 per group). At week 6, a mean increase of 1.57, 2.22, and 2.92 g/dL was observed with desidustat 100, 150 and 200 mg, respectively, versus 0.46 g/dL with placebo in the mITT population (primary endpoint). Haemoglobin response rates (haemoglobin increase of ≥ 1 g/dL from baseline to week 6) in the mITT population were 66%, 75% and 83% with desidustat 100, 250 and 200 mg, respectively, versus 23% with placebo [12].
2.3.3 COVID-19
Desidustat treatment increased red blood cell production and improved oxygen delivery to tissues in patients with COVID-19 infection who were participating in a randomized, open-label, comparator-controlled, phase 2b study (NCT04463602) [15]. None of the hospitalized patients receiving desidustat compared with 25% of patients receiving standard of care treatment required mechanical ventilation. These results suggest that treatment with desidustat could potentially help to prevent acute respiratory distress syndrome in patients with COVID-19 [15].
2.4 Adverse Events
Desidustat was generally well tolerated in the pivotal phase 3 DREAM-D [14] and DREAM-ND [13] studies in patients with anaemia of CKD who were (NCT04215120) [14] or were not (NCT04012957) [13] on dialysis.
In DREAM-D in patients with anaemia due to dialysis-dependent CKD, the incidence of treatment-emergent adverse events (AEs) was similar between patients receiving desidustat and those receiving epoetin alfa (48% vs 46%) [14]. The majority of AEs were mild in severity, unrelated to treatment and resolved without dosage modification in either treatment group. The most common (incidence > 4%) AEs in desidustat and epoetin alfa groups were pyrexia (8.2% vs 5.1%), vomiting (4.1% vs 3.6%), asthenia (4.1% vs 3.6%), headache (3.6% vs 4.6%) and dyspnoea (2.6% vs 4.6%). Serious AEs occurred in 8.2% of desidustat and 10.7% of epoetin alfa recipients, with the most common event being infection and infestation (4.1% vs 3.6%); no serious AE was considered treatment related. No treatment related deaths were reported in either treatment group. At baseline, the majority of patients in the desidustat (92.4%) and epoetin alfa (90.8%) groups had comorbid hypertension [mean systolic blood pressure (BP) ≈ 143 mmHg and diastolic BP ≈ 82 mmHg]. At week 26, no clinically significant change from baseline in sitting systolic BP (mean change − 4.8 vs – 4.6 mmHg) or sitting diastolic BP (− 1.8 vs − 1.0 mmHg) was observed with desidustat or epoetin alfa [14].
Key clinical trials of desidustat sponsored by Zydus Cadila
Drug(s) | Indication | Phase | Status | Location(s) | Identifier |
---|---|---|---|---|---|
Desidustat, epoetin alfa | CKD on dialysis | 3 | Completed | India | DREAM-D; NCT04215120; DESI.19.001.01 |
Desidustat, darbepoetin alfa | CKD not on dialysis | 3 | Completed | India | DREAM-ND; NCT04012957; DESI.18.001 |
Desidustat, Placebo | CKD not on dialysis | 3 | China | ChiCTR2100052908 | |
Desidustat, placebo | CKD not on dialysis | 2 | Completed | India | CTRI/2017/05/008534 |
Desidustat, standard of care | COVID-19 | 2 | Completed | Mexico | NCT04463602; DESI.20.004 |
Desidustat | CKD on dialysis | 1b/2a | Completed | India | CTRI2018-08-015307 |
Desidustat | Chemotherapy induced anaemia | 1 | Completed | India | NCT04667533; DESI.20.001 |
In DREAM-ND in patients with anaemia due to non-dialysis-dependent CKD, the incidence of treatment-emergent AEs was similar between patients receiving desidustat and those receiving darbepoetin alfa (48% vs 50%) [13]. The majority of AEs were mild in severity, unrelated to treatment and resolved in both treatment groups. The most common (incidence > 4%) AEs in desidustat and darbepoetin alfa groups were pyrexia (6.8% vs 6.8%), peripheral oedema (5.4% vs 3.1%), headache (3.7% vs 4.1%) and hypertension (1.7% vs 5.8%). Hyperkalaemia occurred in < 2% of patients in the desidustat and darbepoetin alfa groups (1.0% vs 1.7%). Serious AEs occurred in 8.2% of desidustat and 6.1% of darbepoetin alfa recipients, with the most common event being infection and infestation (4.8% vs 1.4%); no serious AE was considered treatment related. No treatment related deaths were reported in either treatment group. One patient withdrew from treatment in the desidustat due to an AE (diabetic foot infection), which was considered unrelated to treatment. At baseline, the majority of patients in the desidustat (85.0%) and darbepoetin alfa (82%) groups had comorbid hypertension [mean systolic BP ≈ 133 mmHg and diastolic BP ≈ 81 mmHg]. At week 26, no clinically significant change from baseline in sitting systolic (mean change − 0.94 vs + 0.31 mmHg) or sitting diastolic BP (− 0.22 vs + 0.11 mmHg) was observed with desidustat or darbepoetin alfa. Clinically significant abnormal electrocardiogram results were reported in one patient in the desidustat group and six patients in the darbepoetin alfa group [13].
3 Ongoing Trials
A randomized, double-blind, placebo-controlled, phase 3 trial (ChiCTR2100052908) is planned that will evaluate the efficacy and safety of desidustat in ≈ 150 patients with anaemia due to non-dialysis-dependent CKD in China.
References
Mima A. Hypoxia-inducible factor-prolyl hydroxylase inhibitors for renal anemia in chronic kidney disease: advantages and disadvantages. Eur J Pharmacol. 2021;912:174583.
Weir MR. Managing anemia across the stages of kidney disease in those hyporesponsive to erythropoiesis-stimulating agents. Am J Nephrol. 2021;52(6):450–66.
Bonomini M, Del Vecchio L, Sirolli V, et al. New treatment approaches for the anemia of CKD. Am J Kidney Dis. 2016;67(1):133–42.
Sanghani NS, Haase VH. Hypoxia-inducible factor activators in renal anemia: current clinical experience. Adv Chronic Kidney Dis. 2019;26(4):253–66.
Zydus Cadila. Zydus to launch OxemiaTM (desidustat) a breakthrough treatment for anemia in patients suffering from chronic kidney disease (CKD) [media release]. 7 Mar 2022. https://www.zyduslife.com/public/pdf/pressrelease/Press_Release_Zydus_to_launch_Oxemia_a_breakthrough_treatment_for_Anemia_in_patients_suffering_from_CKD.pdf.
Zydus Lifesciences Ltd. OxemiaTM (desidustat): summary of product characteristics. Ahmedabad: Zydus Lifesciences Ltd.; 2022.
Zydus Cadila. Zydus and China Medical System Holdings enter into a license agreement for desidustat in Greater China [media release]. 20 Jan 2020. https://www.zyduslife.com/public/pdf/pressrelease/Zydus_and_China_Medical_System_Holdings_enter_into_a_License_Agreement_for_Desidustat_in_Greater_China.pdf.
Jain MR, Joharapurkar AA, Pandya V, et al. Pharmacological characterization of ZYAN1, a novel prolyl hydroxylase inhibitor for the treatment of anemia. Drug Res (Stuttg). 2016;66(2):107–12.
Patel H, Joharapurkar AA, Pandya VB, et al. Influence of acute and chronic kidney failure in rats on the disposition and pharmacokinetics of ZYAN1, a novel prolyl hydroxylase inhibitor, for the treatment of chronic kidney disease-induced anemia. Xenobiotica. 2018;48(1):37–44.
Jain M, Joharapurkar A, Patel V, et al. Pharmacological inhibition of prolyl hydroxylase protects against inflammation-induced anemia via efficient erythropoiesis and hepcidin downregulation. Eur J Pharmacol. 2019;843:113–20.
Kansagra KA, Parmar D, Jani RH, et al. Phase I clinical study of ZYAN1, a novel prolyl-hydroxylase (PHD) inhibitor to evaluate the safety, tolerability, and pharmacokinetics following oral administration in healthy volunteers. Clin Pharmacokinet. 2018;57(1):87–102.
Parmar DV, Kansagra KA, Patel JC, et al. Outcomes of desidustat treatment in people with anemia and chronic kidney disease: a phase 2 study. Am J Nephrol. 2019;49(6):470–8.
Agrawal D, Varade D, Shah H, et al. Desidustat in anemia due to non-dialysis-dependent chronic kidney disease: a phase 3 study (DREAM-ND). Am J Nephrol. 2022. https://doi.org/10.1159/000523961.
Gang S, Khetan P, Varade D, et al. Desidustat in anemia due to dialysis-dependent chronic kidney disease: a phase 3 study (DREAM-D). Am J Nephrol. 2022. https://doi.org/10.1159/000523949.
Zydus Cadila. Zydus' Desidustat shows efficacy and safety in treating Hypoxia in hospitalized COVID-19 patients in Mexico [media release]. 25 Jan 2021. https://www.zyduslife.com/public/pdf/pressrelease/Zydus_%20Desidustat_shows_efficacy_and_safety_in_treating_Hypoxia_in_hospitalized_Covid_19_patients_in_Mexico.pdf.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Funding
The preparation of this review was not supported by any external funding.
Authorship and conflict of interest
During the peer review process the manufacturer of the agent under review was offered an opportunity to comment on the article. Changes resulting from any comments received were made by the authors on the basis of scientific completeness and accuracy. Sohita Dhillon is a contracted employee of Adis International Ltd/Springer Nature and declares no relevant conflicts of interest. All authors contributed to the review and are responsible for the article content.
Ethics approval, Consent to participate, Consent to publish, Availability of data and material, Code availability
Not applicable.
Additional information
This profile has been extracted and modified from the AdisInsight database. AdisInsight tracks drug development worldwide through the entire development process, from discovery, through pre-clinical and clinical studies to market launch and beyond.
Supplementary Information
Below is the link to the electronic supplementary material.
Rights and permissions
About this article
Cite this article
Dhillon, S. Desidustat: First Approval. Drugs 82, 1207–1212 (2022). https://doi.org/10.1007/s40265-022-01744-w
Published:
Issue Date:
DOI: https://doi.org/10.1007/s40265-022-01744-w