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Last update 08 May 2025

NFE2

Last update 08 May 2025

Basic Info

Synonyms

Leucine zipper protein NF-E2, NF-E2, NFE2

+ [4]

Introduction

Component of the NF-E2 complex essential for regulating erythroid and megakaryocytic maturation and differentiation. Binds to the hypersensitive site 2 (HS2) of the beta-globin control region (LCR). This subunit (NFE2) recognizes the TCAT/C sequence of the AP-1-like core palindrome present in a number of erythroid and megakaryocytic gene promoters. Requires MAFK or other small MAF proteins for binding to the NF-E2 motif. May play a role in all aspects of hemoglobin production from globin and heme synthesis to procurement of iron.

Drugs associated with NFE2

TFM-735

Target

KEAP1 x NFE2

Mechanism

KEAP1 modulators [+1]

Active Org.

Mochida Pharmaceutical Co., Ltd. [+1]

Originator Org.

Mochida Pharmaceutical Co., Ltd.

Active Indication

Multiple Sclerosis

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

KTX 201 (Kuria Therapeutics)

Target

NFE2

Mechanism

NFE2 stimulators

Active Org.

Kuria Therapeutics, Inc.

Originator Org.

Kuria Therapeutics, Inc.

Active Indication

Eye Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

KTX-301

Target

NFE2

Mechanism

NFE2 stimulators

Active Org.-

Originator Org.

Kuria Therapeutics, Inc.

Active Indication-

Inactive Indication

Skin Diseases

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NFE2

100 Translational Medicine associated with NFE2

0 Patents (Medical) associated with NFE2

654

Literatures (Medical) associated with NFE2

01 Apr 2025·Journal of Medicinal Food

The Therapeutic Role of Saffron and Its Components Mediated Through Nrf2 in Diabetes and Related Pathologies

Review

Author: Alemzadeh, Effat ; Samini, Fariborz ; Farkhondeh, Tahereh ; Majidpour, Mahdi ; Samarghandian, Saeed ; Aschner, Michael ; Sabeti Akbar-Abad, Mahboobeh

Today, diabetes is considered a growing global epidemic. In the diabetic environment, a large amount of reactive oxygen species are produced. This type of active oxygen causes severe damage to cell membranes, proteins, and DNA. Therefore, finding a solution to deal with and reduce this type of reactive oxygen is very important. One of the most effective ways to deal with oxidative damage and inflammation is the modulation of the nuclear factor erythroid 2 (Nrf2) signaling pathway. One of the useful natural substances that can be used for treatment in the signaling system is saffron. In this article, research evaluating the medicinal effects of saffron and its compounds and their mechanisms of action, especially the Nrf2 signaling pathway, have been investigated and studied. The results show that saffron and its components have the potential to treat diabetes due to their unique properties.

01 Mar 2025·Journal of Ethnopharmacology

Total flavonoids extracted from the leaves of Murraya paniculata (L.) Jack prevents acetaminophen-induced liver injury by activating Keap1/Nrf2 and PI3K/AKT/mTOR signaling pathway

Article

Author: Li, Tianlang ; Zuo, Shunfang ; Xu, Huali ; Zhang, Zihao ; Feng, Shuting ; Zhang, Xiaoze ; Wang, Huifeng ; Wang, Zhanpeng ; Fu, Wenwen ; Ma, Wenli ; Wang, Xinjie ; Guo, Meiqi ; Sun, Han

ETHNOPHARMACOLOGICAL RELEVANCEIn regions such as China and Southeast Asia, leaves of the traditional Chinese medicinal herb Murraya paniculata (L.) Jack are highly valued for their ability to detoxify and reduce swelling, promote blood circulation, and alleviate pain. These properties are harnessed in traditional healing practices, where the herb is aligned with the liver and stomach meridians in Chinese medicine. Consequently, extracts from the leaves of Murraya paniculata (L.) Jack are believed to ameliorate various liver-related ailments. Despite its widespread use, there is a paucity of research demonstrating the protective effect of total flavonoids extracted from the leaves of Murraya paniculata (L.) Jack (TFMP) in relieving acetaminophen-induced acute liver injury (ALI).AIM OF THE STUDYThis study aimed to investigate the hepatoprotective effects and probable mechanisms of action of TFMP in acetaminophen-induced acute liver damage.MATERIALS AND METHODSExperimental animals were randomized into four groups of 10 each and then orally pretreated with 0.5% carboxymethyl cellulose or TFMP for seven consecutive days. ALI was induced using acetaminophen (APAP, 300 mg/kg). Hematoxylin and eosin (H&E) staining and serum markers were used to evaluate liver damage. Immunofluorescence, western blotting, biochemical kit testing, immunohistochemistry, and qPCR were used to evaluate acetaminophen metabolism, oxidative damage, and hepatocyte death.RESULTSTFMP considerably lowered the liver-related transaminase activity and reduced pathological liver damage. By triggering the kelch-like ECH-associated protein 1 (Keap1)/nuclear erythroid related factor 2 (Nrf2) signaling pathway in hepatic tissue, antioxidative enzymes, such as superoxide dismutase (SOD) and catalase (CAT), and glutathione (GSH) were elevated and malondialdehyde (MDA) content was diminished. Based on western blotting and immunohistochemistry examinations, TFMP could boost Nrf2 accumulation within liver tissue and modulate Nrf2 entry into the nucleus, increasing the proteins involved in heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) expression. Furthermore, TFMP promoted the expression of the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) while reducing the expression of pro-apoptotic proteins such as Bcl2-associated X (Bax). Overall, TFMP attenuated hepatocyte apoptosis by activating the PI3K/AKT/mTOR pathway.CONCLUSIONThis study shows that TFMP reduces APAP-induced acute liver damage by a mechanism that affected the APAP metabolic process in vivo and activated the PI3K/AKT/mTOR and Keap1/Nrf2 signaling pathways to exert anti-apoptotic and antioxidant effects. Thus, TFMP may be a viable option for preventing APAP-induced liver damage.

01 Feb 2025·Annales de Biologie Clinique

Multi-omics analysis reveals the molecular mechanisms and therapeutic targets in high altitude polycythemia

Article

Author: Wang, Chengwen ; Wang, Minghui ; Li, Yanyan ; Ma, Haiyan

Polycythemia, characterized by an abnormal increase in red blood cells, can manifest as primary polycythemia (PV) or secondary polycythemia, often due to conditions like obstructive sleep apnea (OSA) and high-altitude polycythemia (HAP). Understanding the molecular mechanisms underlying these conditions is crucial for developing targeted therapies. Transcriptome analysis was performed to identify differentially expressed genes (DEGs), significant modules, and immune cell infiltration. We identified 370 DEGs and four significant gene co-expression modules closely related to HAP. Modules were associated with neutrophil migration, glycoprotein metabolism, UDP-N-acetylglucosamine synthesis, and red pulp cells. These modules showed the same directions of change in OSA but were reversed when treated with continuous positive airway pressure therapy. Comparison with GWAS showed that overlapping genes were related to oxygen transport in the DEGs. PRDM1 and NCOA1, NFE2 were identified as key transcription factors. Noca1 knockout mice showed elevated levels of red blood cell count (RBC), hemoglobin (HGB), and hematocrit (HCT). Lomustine and hydralazine emerged as potential candidate drugs for treating polycythemia. Abdominal breathing training for three months improved symptoms and reduced RBC, HGB, and HCT in 33 HAP patients. These findings elucidate HAP's molecular mechanisms and suggest new therapeutic directions.

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