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Last update 08 May 2025

CYP24A1

Last update 08 May 2025

Basic Info

Synonyms

1,25-dihydroxyvitamin D(3) 24-hydroxylase, mitochondrial, 24-OHase, CP24

+ [10]

Introduction

A cytochrome P450 monooxygenase with a key role in vitamin D catabolism and calcium homeostasis. Via C24- and C23-oxidation pathways, catalyzes the inactivation of both the vitamin D precursor calcidiol (25-hydroxyvitamin D(3)) and the active hormone calcitriol (1-alpha,25-dihydroxyvitamin D(3)) (PubMed:11012668, PubMed:15574355, PubMed:16617161, PubMed:24893882, PubMed:29461981, PubMed:8679605). With initial hydroxylation at C-24 (via C24-oxidation pathway), performs a sequential 6-step oxidation of calcitriol leading to the formation of the biliary metabolite calcitroic acid (PubMed:15574355, PubMed:24893882). With initial hydroxylation at C-23 (via C23-oxidation pathway), catalyzes sequential oxidation of calcidiol leading to the formation of 25(OH)D3-26,23-lactone as end product (PubMed:11012668, PubMed:8679605). Preferentially hydroxylates at C-25 other vitamin D active metabolites, such as CYP11A1-derived secosteroids 20S-hydroxycholecalciferol and 20S,23-dihydroxycholecalciferol (PubMed:25727742). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via FDXR/adrenodoxin reductase and FDX1/adrenodoxin (PubMed:8679605).

Drugs associated with CYP24A1

CN117003679

Patent Mining

Target

CYP24A1

Mechanism

CYP24A1 inhibitors

Active Org.

University of South Australia

Originator Org.

University of South Australia

Active Indication

Digestive System Disorders [+4]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

RC-8800

Target

CYP24A1 x VDR

Mechanism

CYP24A1 inhibitors [+2]

Active Org.-

Originator Org.

Helsinn Healthcare SA

Active Indication-

Inactive Indication

Prostatic Cancer

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Lunacalcipol

Target

CYP24A1 x VDR

Mechanism

CYP24A1 inhibitors [+1]

Active Org.-

Originator Org.

OPKO Health, Inc.

Active Indication-

Inactive Indication

Chronic Kidney Diseases [+4]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with CYP24A1

NCT01453634

/ WithdrawnPhase 2

A Randomized, Open Label, Four Week, Pharmacodynamic/Pharmacokinetic, Efficacy, and Safety Study of Lunacalcipol (CTA018) Injection in Subjects With Stage 5 Chronic Kidney Disease With Secondary Hyperparathyroidism on Hemodialysis

Open-label, pharmacodynamic, safety, pharmacokinetic and efficacy study of Lunacalcipol Injection.

Start Date01 Jan 2013

Sponsor / Collaborator

OPKO Health, Inc.

NCT00742716

/ CompletedPhase 2

An Open Label, Four Week, Dose Escalating Pharmacokinetic, Pharmacodynamic, Efficacy and Safety Study of CTA018 Injection in Subjects With Stage 5 Chronic Kidney Disease With Secondary Hyperparathyroidism on Hemodialysis

This study will investigate the levels of CTA018 in the body over time (pharmacokinetics, PK) in patients with chronic kidney disease (CKD) and secondary hyperparathyroidism (SHPT), undergoing regular hemodialysis. This study will also investigate the safety and effects of different strengths of CTA018, on parathyroid hormone (PTH) levels.

Start Date01 Oct 2008

Sponsor / Collaborator

OPKO IP Holdings II, Inc.

NCT00384098

/ CompletedPhase 2

A Randomized, Double-blind, Parallel-group, 4-arm, 12-week Study to Evaluate the Safety and Efficacy of Topically Applied CTA018 vs Vehicle for the Treatment of Adult Subjects With Chronic Plaque Psoriasis

Vitamin D and its analogs are currently widely used for the treatment of psoriasis. The study drug (CTA018) is a novel analog of vitamin D, and this Phase 2 study will investigate the efficacy and safety of CTA018 in the treatment of psoriasis. Patients with chronic plaque psoriasis will receive one of three doses of CTA018 cream or vehicle (no study drug) daily for 12 weeks.

Start Date01 Sep 2006

Sponsor / Collaborator

OPKO Health, Inc.

100 Clinical Results associated with CYP24A1

100 Translational Medicine associated with CYP24A1

0 Patents (Medical) associated with CYP24A1

1,388

Literatures (Medical) associated with CYP24A1

01 Jun 2025·Steroids

Genetic insights into vitamin D deficiency: a case-control study of GC and CYP24A1 gene polymorphism

Article

Author: Mansour, Lamjed ; Ali, Aktar ; Abbas, Khurram ; Khan, Aslam ; Imran, Muhammad ; Usama ; Raza, Muhammad Kashif

Despite the sunny climate, vitamin D deficiency is highly prevalent in several parts of the world. Several risk factors are associated with VD deficiency, including single nucleotide polymorphism and post-translational modifications in its transport protein, known as vitamin D binding protein (DBP) or GC and CYP24A1, a protein associated with its degradation. Our study explores the impact of rs4588 and rs7041 in the GC gene, along with CYP24A1 rs4809960 and rs2585428, on serum vitamin D and the risk of vitamin D insufficiency. This study enrolled 114 healthy controls and 239 vitamin D-deficient subjects. SNPs were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The G/T genotype of D432E and the A/A genotype of T436K in the GC gene were observed to be risk factors for vitamin D deficiency. Overall, a significant (P < 0.05) association was observed between the D432E and T436K polymorphism and vitamin D deficiency. Polymorphic genotypes of CYP24A1 rs4809960 and rs2585428 polymorphisms were significantly associated with a higher risk of Vitamin D deficiency. D432E and T436K polymorphisms were associated with decreased vitamin D and increased PTH levels in vitamin D-deficient individuals. Similarly, both CYP24A1 polymorphisms were significantly associated with a higher risk of vitamin D deficiency. Also, a negative association was observed between sufficient serum levels of 25-hydroxyvitamin D and PTH levels.

01 Jun 2025·Toxicon

The DHCR7 is the key target of lipotoxic liver injury caused by matrine through abnormal activation of the cholesterol synthesis pathway

Article

Author: Li, Jiaqi ; Zhang, Wenting ; Tao, Xiaoyu ; Li, Zhiqi ; Zhao, Chongjun ; Fan, Qiqi ; Gao, Yifei ; Chen, Linzhen ; Wu, Jiarui ; Lu, Shan

BACKGROUNDMatrine, the main active ingredient in Sophora flavescens and Sophorae tonkinensis radix et rhizome, is a highly effective insecticide. However, its hepatotoxicity to some extent affects its application value. This study aimed to explore the mechanism underlying matrine-induced liver injury.METHODSThe zebrafish (Danio rerio) and L02 cell model were utilized to investigate the toxic dose of matrine and its effects on liver tissue damage, liver cell morphology and activity, and expression levels of ALT and AST. Zebrafish and L02 cell samples were then collected for transcriptomic testing to further explore the possible mechanism by which matrine induced liver injury. Finally, integrated bioinformatics methods and experiments were used to elucidate the possible mechanisms behind matrine-induced liver injury.RESULTSThe result presented solid in vivo evidence of matrine-induced hepatotoxicity, supported by abnormal changes of liver morphological, disturbed liver cell structure, obvious apoptosis, as well as elevated levels of ALT and AST in zebrafish. In addition, in vitro L02 cell experiments also showed that matrine can produce significant liver cell damage effects. The integrated bioinformatics analysis results revealed that differentially expressed genes (DEGs) were substantially enriched in multiple pathways related to lipid regulation. Among which, the steroid biosynthesis was the most key signaling pathway, evidenced by the enhanced expression of eight genes, including DHCR7, SQLE, CYP51, CYP24A1, SC5D, LSS, MSMO1 and SOAT1. Furthermore, AY9944, the targeted inhibitor of DHCR7, could offset the toxic effect, as reflected by diminished liver phenotype damage, steatosis, and cholesterol accumulation caused by matrine.CONCLUSIONSMatrine can upregulate the expression of key genes in steroid biosynthesis pathway, resulting in cholesterol accumulation and then inducing hepatotoxicity. Among them, targeted inhibition of DHCR7 gene expression can alleviate matrine-induced liver injury.

01 Jun 2025·The Journal of Steroid Biochemistry and Molecular Biology

Kidney deletions of Cyp27b1 fail to reduce serum 1,25(OH)2D3

Article

Author: Lee, Seong Min ; Jones, Glenville ; Kaufmann, Martin ; Cichanski, Shannon R ; Meyer, Mark B ; Pintozzi, Nicolas G

Vitamin D metabolism is controlled through the kidney mitochondrial P450 enzymes 1α-hydroxylase (CYP27B1) and 24-hydroxylase (CYP24A1) that activate and degrade the endocrine vitamin D hormone (1,25(OH)₂D₃), respectively. We recently demonstrated that extrarenal cells can make 1,25(OH)₂D₃ with adequate vitamin D supplementation by targeted mass spectrometry imaging in our Cyp27b1 kidney enhancer deletion mouse model that lacks circulating 1,25(OH)₂D₃ (M1/M21-DIKO mouse). Based on these observations, we selectively deleted Cyp27b1 (Cyp27b1^fl/fl) from the mouse kidney using the Six2- and Pax8-cre drivers that target tubule and nephron development to see if we could recapitulate the remarkable phenotype of the M1/M21-DIKO mice. While Six2-cre/Cyp27b1^fl/fl mice had a mild phenotype, Pax8-cre/Cyp27b1^fl/fl mice had a marked elevation of parathyroid hormone and a reduction in bone mineral density. The vitamin D metabolic profile in the Pax8-cre/Cyp27b1^fl/fl clearly indicated a dysfunction in the CYP24A1 enzyme with reductions in 24,25(OH)₂D₃ and 25(OH)D₃-26,23-lactone with an accompanying elevation of 25(OH)D₃. However, despite these compensatory reductions in CYP24A1 derived metabolites and apparent deletion of Cyp27b1 in the kidney, the 1,25(OH)₂D₃ levels were not changed from wildtype in either mouse. Like 24,25(OH)₂D₃, the 1,24,25(OH)₃D₃ levels were also reduced. These data highlight the robust homeostatic mechanisms to salvage 1,25(OH)₂D₃, point towards potential compensatory mechanisms of 1,25(OH)₂D₃ production from non-kidney tissues, and reinforce the utility of the M1/M21-DIKO model as a non-global deletion of Cyp27b1 with reductions in serum 1,25(OH)₂D₃ to be used to understand the complexity of vitamin D metabolism in health and inflammatory disease.

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CYP24A1

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