Request Demo

Last update 08 May 2025

CaN x NFATC1

Last update 08 May 2025

Basic Info

Related Targets

CaNNFATC1

Drugs associated with CaN x NFATC1

AIK-5

Target

CaN x NFATC1

Mechanism

CaN inhibitors [+1]

Active Org.-

Originator Org.

Allinky Biopharma SL

Active Indication-

Inactive Indication

Autoimmune Diseases [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with CaN x NFATC1

JPRN-UMIN000008751

/ CompletedNot Applicable

Multicenter study of combination therapy using calcineurin inhibitor, basiliximab, mizoribine and steroids in kidney transplantation. - Multi-drug combination therapy in kidney transplantation.

Start Date01 Jan 2009

Sponsor / Collaborator-

100 Clinical Results associated with CaN x NFATC1

100 Translational Medicine associated with CaN x NFATC1

0 Patents (Medical) associated with CaN x NFATC1

487

Literatures (Medical) associated with CaN x NFATC1

01 Aug 2025·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

IL-10 alleviates aTCMR by inhibiting NFATc1 signaling pathway of T cells after kidney transplantation

Article

Author: Guo, Ning ; Zhao, Peng ; Peng, Zhi-Guo ; Sun, Huai-Bin ; Liu, Sheng-Li ; Zhou, Yan-Man ; Cui, Xian-Quan

The cause of acute T cell-mediated rejection (aTCMR) is believed to be immune hyperfunction of T cells after kidney transplantation. Nowadays, calcineurin inhibitors are widely used to inhibit the proliferation of T cells when aTCMR occurs. However, the therapeutic dose window of these drugs is relatively narrow and long time use of these drugs may lead to serious side effects. Besides, whether IL-10, a new immune tolerance mediator, playing a therapeutic role on aTCMR remains unclear. The level of IL-10 decreased in patients with aTCMR, suggesting that IL-10 may be involved in the progression of aTCMR. IL-10 could inhibit the proliferation and metabolism of T cells in vitro and in vivo, accompanied by reducing the levels of IL-2, IFN-γ, and TNF-α. Moreover, we confirmed that IL-10 exerts immunosuppressive effects by inhibiting the NFATc1 signaling pathway of T cells. This viewpoint may provide a new therapeutic idea for clinical application.

01 May 2025·Pathology - Research and Practice

Knockout of Trpc6 attenuates T2DM-induced liver injury and inflammation by inhibiting CN-NFAT2-NLRP3 signalling in mice

Article

Author: Wang, Guohang ; Liu, Yan ; Li, Weiping ; Xu, Hanyang ; Su, Yong ; Sun, Ran ; Li, Weizu ; Zhou, Huimin ; Ji, Pengmin ; Fu, Yinglin

Diabetic liver disease is a common complication of diabetes mellitus that poses significant harm to patients. Transient receptor potential cation channel 6 (TRPC6) is a non-selective cation channel with calcium permeability, playing a key role in signalling pathways associated with liver disease progression. This study aimed to investigate the effects of Trpc6 knockout on liver injury and its regulation of the calcineurin (CN)-nuclear factor of activated T cells 2 (NFAT2) signalling pathway in mice with type 2 diabetes mellitus (T2DM). Serum aspartate aminotransferase and alanine aminotransferase levels were measured to assess liver function, while haematoxylin and eosin staining, periodic acid-Schiff staining, and Masson staining were used to evaluate pathological injury. Nile Red and Oil Red O staining were performed to assess hepatic lipid deposition. Western blotting, quantitative real-time polymerase chain reaction, and immunohistochemistry were used to analyse fibrosis- and inflammation-related markers in mouse liver tissues. The results showed that Trpc6 knockout had no significant effect on hepatic lipid deposition, CD36 expression, or phosphorylated phospholipase C levels in the liver tissues of mice with T2DM. However, Trpc6 knockout significantly inhibited NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome activation, thereby alleviating liver injury and fibrosis in mice with T2DM. Further findings indicated that Trpc6 knockout markedly reduced CN and NFAT2 expression in T2DM liver tissues and resisted intracellular calcium overload in liver cells in vitro. This study suggests that Trpc6 knockout attenuates T2DM-induced hepatic inflammation and fibrosis by inhibiting hepatocyte calcium overload and suppressing the CN-NFAT2-NLRP3 signalling pathway.

01 May 2025·European Journal of Pharmacology

Tropisetron attenuates high-glucose-induced vascular endothelial dysfunction via inhibition of calcineurin/NFAT signalling

Article

Author: Ghaffari-Bohlouli, Pejman ; Nadjafi, Shabnam ; Dehpour, Ahmad Reza ; Shafiei, Massoumeh ; Barzegar-Fallah, Anita ; Alimoradi, Houman ; Razmi, Ali ; Ghaffarian-Bahraman, Ali

Vascular endothelial dysfunction (VED) is considered an important initiating factor in pathogenesis of diabetic vascular disease. In this process, oxidative insult, cellular hypertrophy, and activation of the calcineurin/nuclear factor of activated T-cell (NFAT) pathway play key roles. Herein, we investigated the effects of tropisetron (TRS), a calcineurin inhibitor, on high glucose (HG)-induced hypertrophy and apoptosis in human umbilical vein endothelial cells (HUVECs). To this end, HUVECs and chorioallantoic membranes (CAMs) were exposed to HG with or without TRS or cyclosporine A (CsA), and the effects of the treatments were evaluated on oxidative stress generation, cell number (proliferation and apoptosis), cell size (hypertrophy), and vessel formation. We also explored the possible role of calcineurin-NFAT signalling in the potential protective effects of TRS on hypertrophy and apoptosis associated with HG. The average size and protein content of the cells exposed to HG for 48h were significantly increased compared with normal glucose (NG). HG significantly increased apoptosis, altered the cell cycle, and elevated oxidative and nitrosative stress in HUVECs. Further, exposing cells to HG resulted in elevated calcineurin activity and NFATc1 translocation to the nuclei. HG also caused a significant decrease in the formation of new blood vessels in CAMs. Inhibition of calcineurin/NFAT pathway by TRS or CsA protected against these pathological changes. Our data demonstrated that inhibition of calcineurin/NFAT signalling by TRS, as a safe calcineurin inhibitor, may ameliorate HG-induced VED. Further in vivo and clinical studies are required to fully determine the protective effects of TRS against VED in diabetes.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis