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Last update 08 May 2025

ANXA3

Last update 08 May 2025

Basic Info

Synonyms

35-alpha calcimedin, annexin A3, Annexin III

+ [7]

Introduction

Inhibitor of phospholipase A2, also possesses anti-coagulant properties. Also cleaves the cyclic bond of inositol 1,2-cyclic phosphate to form inositol 1-phosphate.

Drugs associated with ANXA3

ANXA3 inhibitors(Fudan University)

Target

ANXA3

Mechanism

ANXA3 inhibitors

Active Org.

Fudan University

Originator Org.

Fudan University

Active Indication

Triple Negative Breast Cancer

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ANXA3

100 Translational Medicine associated with ANXA3

0 Patents (Medical) associated with ANXA3

379

Literatures (Medical) associated with ANXA3

01 Dec 2025·Immunologic Research

The effect of anti-CD20 on inflammation and histopathological alternations in rat photothrombotic ischemic stroke model

Article

Author: Athari, Seyed Zanyar ; Babaei, Fatemeh ; Pirouzpanah, Mohammad Bagher ; Abolhasanpour, Nasrin ; Delkhosh, Aref ; Mehdizadeh, Amir ; Dolati, Sanam ; Soltani-Zangbar, Mohammad Sadegh ; Yousefi, Mehdi ; Hosseini, Leila ; Rikhtegar, Reza ; Hosseini, Maryam ; Alikhaniha, Hossein

Ischemic stroke (IS) has remained the main cause of mortality and neurological disabilities worldwide. Anti-CD20 treatments have a potent anti-inflammatory effect. Here, we investigated the effect of anti-CD20 on IS-induced inflammation and histopathologic changes in the rat model. Male Sprague-Dawley rats were divided into three groups: control, sham, and stroke. Rats in the stroke groups underwent photothrombosis-induced IS in the sensorimotor cortex area. They were divided into the following subgroups: treated with anti-CD20 after ischemia and killed after 5 and/or 10 days of IS. Histological changes were assessed by hematoxylin and eosin staining. mRNA levels of inflammation markers (VIM, ANXA3, SLC22 A4, and ADM), and also levels of transcription factors for Th1, Th2, and Th17 subsets (Tbet, GATA3, and ROR-γ, respectively), and also Foxp3 were detected in the peripheral blood mononuclear cells by quantitative real-time PCR. The levels of ADM and SLC22 A4 increased following IS on the 5th and 10th days, while treatment with anti-CD20 reversed their levels. Anti-CD20 therapy attenuated inflammation through down-regulation of VIM and ANXA3 after 10 days. This therapeutic effect was mainly mediated by the downregulation of Th1-Th17-driven inflammatory responses (Tbet and RORγt) and the upregulation of Th2 activities (GATA- 3). In addition, anti-CD20 increased the expression of Foxp3. Anti-CD20 treatment can also reduce brain tissue damage after 10 days. Our data showed that inflammation and histopathological alterations are associated with the photothrombotic model of IS, while treatment with anti-CD20 could reduce inflammation and alleviate histopathological changes.

01 Apr 2025·International Immunopharmacology

Impact of gold nanoparticle exposure on the development pancreas and kidney: Dose-dependent;oxidative stress; miRNA expression and Nrf2/ARE Signalling

Article

Author: Alghamdi, Mansour Abdullah ; Zafrah, Hind ; Al-Zahrani, Norah Saeed ; El Henafy, Hanan M A ; El Nasha, Eman Mohamad

BACKGROUNDThe widespread use of gold nanoparticles (AuNPs) in consumer and medical products necessitates investigation into their potential developmental toxicity.AIM OF THE WORKThis study investigated the systemic effects of in-utero AuNP exposure on developing male rat offspring, focusing on metabolic, organ-specific, and cellular pathways.MATERIALS AND METHODSPregnant rats were intravenously administered AuNPs (5, 10, 15, or 20 mg/kg) or saline from gestational day 1 to birth. Male offspring were assessed at postnatal day 60 through biochemical and genetic analyses in the pancreas, kidney tissues, plasma analysis, and pancreatic histology.RESULTSNo mortality or clinical abnormalities occurred. However, in-utero AuNP high-dose exposure induced pancreatic abnormalities, including reduced endocrine function and morphological damage. Higher doses disrupt body and organ growth, leading to metabolic dysregulation (elevated glucose, amylase, lipase, reduced insulin), impairing glucose homeostasis, and pancreatic dysfunction. Compromised kidney function (elevated urea, creatinine, BUN, electrolyte imbalances), increased oxidative stress, and dysregulated inflammatory responses (altered TNF-α, IL-6, IL-10, Nrf2, NF-κB) were also observed. AuNPs induced apoptosis (increased caspase-3, decreased Bcl-2, and altered COX-2), as well as dysregulation of mRNA and miRNA expression. Affected genes included those related to stress and inflammation (p-p38, NOX4, iNOS, NF-κB, Akt, mTOR, Anxa3) and cellular survival signalling (miR-21, miR-382, miR-34a, miR-223). Pancreatic histopathology revealed dose-dependent tissue damage.CONCLUSIONThese results indicate that AuNPs, especially at higher doses, disrupt multiple biological processes, inducing metabolic, renal, and pancreatic dysfunction via oxidative stress, inflammation, and cellular dysregulation. Further mechanistic research is crucial to establish safe applications, highlighting the need for biosafety assessments guided by green toxicology principles.

13 Mar 2025·Journal of Medicinal Chemistry

Discovery of a Novel 1,4-Benzodiazepine Derivative as a Highly Selective ANXA3 Degrader for the Treatment of Triple-Negative Breast Cancer

Article

Author: Liu, Kunlin ; Jin, Zijun ; Sun, Xun ; Zhu, Chenhao ; Min, Delin ; Liang, Yongxi

Annexin A3 has been demonstrated to be a key pathogenic protein in the occurrence and development of triple-negative breast cancer (TNBC); its overexpression in TNBC cells can promote the proliferation, migration, and drug resistance of TNBC. Previously, we reported the first ANXA3 degrader, (R)-SL18, with potent anti-TNBC effects, albeit with moderate ANXA3 binding affinity leading to off-target effects and relatively poor degradation selectivity of family proteins. To obtain molecules with stronger binding with ANXA3 and lower toxicity, we performed further structural optimization of (R)-SL18 to explore structure-activity relationships for a series of 1,4-benzodiazepines. Among them, compound 18a5 exhibited a 14-fold increase in ANXA3 binding activity, along with better cancer cell inhibition and functional activity. In particular, 18a5 showed more desirable ANXA3 selective degradation than (R)-SL18 and displayed excellent inhibitory effect in a TNBC tumor xenograft model (TGI = 96%). Collectively, 18a5 proved to be a promising lead compound to treat TNBC through the degradation of ANXA3.

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ANXA3

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