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Last update 08 May 2025

ADAMTS

Last update 08 May 2025

Basic Info

Synonyms-

Introduction-

Drugs associated with ADAMTS

CN117136051

Patent Mining

Target

ADAMTS x ADAMTS4 x ADAMTS5 x ADAMTSL4

Mechanism

ADAMTS inhibitors

Active Org.

Jiangsu Hengrui Pharmaceuticals Co., Ltd.

Originator Org.

Jiangsu Hengrui Pharmaceuticals Co., Ltd.

Active Indication

Inflammation [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ADAMTS

100 Translational Medicine associated with ADAMTS

0 Patents (Medical) associated with ADAMTS

614

Literatures (Medical) associated with ADAMTS

01 Jun 2025·European Journal of Nutrition

Vitamin D deficiency promotes intervertebral disc degeneration via p38/NCoR2-mediated extracellular matrix degradation

Article

Author: Chen, Chao ; Wang, Bing ; He, Qicong ; Wang, Xuenan ; Zhan, Enyu ; Li, Xingguo ; Hu, Yaoquan ; Lv, Zhengpin ; Zhang, Fan

PURPOSEVitamin D (VD) deficiency significantly contributes to intervertebral disc degeneration (IDD), a common cause of low back pain, yet the underlying mechanisms remain unclear. This study investigates how VD deficiency exacerbates IDD and identifies potential therapeutic targets.METHODSWe used real-time quantitative PCR, immunoblots, immunoprecipitation, liquid chromatography with tandem mass spectrometry analysis, co-immunoprecipitation, and chromatin immunoprecipitation to study gene and protein expressions, protein complex assembly, and transcriptional complex binding. Degeneration of IVDs was assessed via hematoxylin and eosin staining.RESULTSEight members of ADAMTSs (A disintegrin and metalloproteinase with thrombospondin motifs) are enriched in lumbar discs of both VD-deficient and VD receptor (VDR)-knockout (VDR^-/-) mice. Sufficient VD suppresses ADAMTS genes through a complex formed by nuclear receptor corepressor 2 (NCoR2) and signal transducer and activator of transcription 6 (STAT6). VD deficiency activates p38 kinase, leading to NCoR2 phosphorylation and subsequent degradation by a Cullin 4-RING (CRL4) E3 ligase, impairing NCoR2's transrepression function and upregulating ADAMTS genes, accelerating extracellular matrix (ECM) degradation in discs. This mechanism is replicated in VDR-deficient cells. In vitro treatments with p38 inhibitor (BIRB-796) and CRL4 inhibitor (KH-4-43) reduce ADAMTS expression, and in vivo application of these inhibitors improves disc integrity in VD-deficient mice.CONCLUSIONOur findings highlight NCoR2 degradation, mediated by p38 kinase and CRL4 E3 ligase, as crucial in VD deficiency-induced IDD. Targeting this pathway offers promising therapeutic potential to mitigate IDD progression in individuals with VD deficiency or VDR abnormalities.

01 Mar 2025·Journal of Cellular and Molecular Medicine

Cartilage Intermediate Layer Protein‐1 Promotes Extracellular Matrix Degeneration via Interacting With CD47

Article

Author: Zhang, Zehua ; Yang, Yusheng ; He, Jinyue ; Xiang, Yu ; Xu, Jianzhong ; Deng, Jiezhong ; Luo, Fei

ABSTRACTIntervertebral Disc Degeneration (IDD) is a multifactorial result contributing to Low Back Pain (LBP) while Cartilage Intermediate Layer Protein‐1 (CILP‐1) is gradually up‐regulated along with IDD. Whether CILP‐1 acts in a direct role promoting IDD via regulating matrix metabolism remains to be elucidated. Herein, we firstly detected the expression level of matrix‐related phenotypes in nucleus pulposus (NP) cells treated with CILP‐1, including ADAMTS, MMPs, IL‐6, Collagens, Aggrecan (ACAN) and SOX9. Meanwhile, the phosphorylation levels of MAPKs and NF‐κB were detected to explore the involved signalling pathways, which were further validated by inhibition experiments. Furthermore, molecular docking analysis was employed to evaluate the possibility of CD47 acting as the direct receptor mediating CILP's regulation above, which was further validated by immunoprecipitation and inhibition experiment. Our findings have made a comprehensive investigation into the regulatory effect of CILP‐1 on the matrix metabolism of NP cells and explored the underlying mechanism.

01 Feb 2025·European Journal of Pharmacology

Targeting Ubiquitin–Proteasome system (UPS) in treating osteoarthritis

Review

Author: Kamarul, Tunku ; Wong, Pooi-Fong

Despite osteoarthritis (OA) being recognised for over a century as a debilitating disease that affects millions, there are huge gaps in our understanding of the underlying pathophysiology that drives this disease. Present day studies that focussed on ubiquitination (Ub) and ubiquitylation-like (Ubl) modification related mechanisms have brought light into the possibility of attenuating OA development by targeting these specific proteins in chondrocytes. In the present review, we discuss recent advances in studies involving Ub ligases and deubiquitinating enzymes (DUBs) which are of importance in the development of OA, and may offer potential therapeutic strategies for OA. Such targets may involve attenuating proteases such as matrix metalloproteinases (MMP) 1, 8, 13, 4 and several A Disintegrin and Metalloproteinase with Thrombospondin Motifs (ADAMTS) that are well known for their roles in cartilage breakdown. Ligases such as ubiquitin-conjugating enzymes (E2) and ubiquitin-ligating enzymes (E3) that are involved in extracellular matrix (ECM) degradation in OA and of their pathogenesis would be discussed. In addition to catabolic and degenerative downstream effects of Ub and DUBs in OA, inflammatory mechanisms most notably involving nuclear factor-kappa B (NF-κB) signalling pathways regulated through Ub and using various targeting molecules would also be highlighted. Challenges, gaps and insights from clinical trials will provide valuable guidance for future investigations on targeting ubiquitin-proteosome system (UPS) as a therapeutic option for OA.

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ADAMTS

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