Target intelligence / Profile preview

Suppressor of inflammatory macrophage apoptosis lncRNA (SIMALR)

Target: SIMALR
Molecular classification: Long noncoding RNA (lncRNA), Long intergenic noncoding RNA (lincRNA), Other (non-protein coding RNA)

Overview

Suppressor of inflammatory macrophage apoptosis lncRNA (SIMALR) is a human-specific long intergenic noncoding RNA (lincRNA) highly expressed in inflammatory “M1-type” macrophages. SIMALR is induced by stimuli such as LPS/IFN-γ and protects these macrophages from apoptosis in part by promoting NTN1 expression via HIF1α-dependent transcriptional regulation. SIMALR plays a critical role in modulating macrophage survival and inflammatory responses within atherosclerotic plaques. Knockdown of SIMALR increases apoptosis in these cells and reduces NTN1 levels; addition of recombinant NTN1 rescues macrophage survival. SIMALR is expressed in macrophages in human carotid atherosclerotic plaques and may represent a novel therapeutic target for modulating inflammatory cell survival in cardiovascular disease[2][3][5][7].

Other names: LINC02528 (gene synonym)

Mechanism of action

SIMALR protects inflammatory macrophages from apoptosis by increasing the transcription of NTN1, a known survival factor for macrophages. SIMALR interacts with HIF1α to facilitate NTN1 promoter activation, thereby increasing macrophage survival during inflammation

Biological functions

Regulation of *macrophage apoptosis* (cell death)*Inflammatory response* modulationProtection of *inflammatory macrophages* from apoptosisPromotes *macrophage survival* in the context of inflammation and atherosclerotic plaques

Disease associations

*Cardiovascular disease* (atherosclerosis)*Inflammation*Potential link to *cancer progression* (recent findings suggest a role in nasopharyngeal carcinoma through post-transcriptional mechanisms, though core function is cardiovascular inflammation)

Safety considerations

Therapeutic targeting of SIMALR could potentially alter inflammation resolution and plaque stability, which must be carefully considered in cardiovascular disease contexts.Unknown off-target effects of RNA-based therapeutics

Interacting drugs

None directly identified; studies have used *SIMALR antisense oligonucleotides* as research tools, but no approved drugs are known to target SIMALR

Biomarkers

*SIMALR expression* in macrophages may serve as a biomarker for inflammatory activity in atherosclerotic plaquesNTN1 levels (functionally downstream of SIMALR, associated with survival of inflammatory macrophages)

Beyond the preview

Go deeper on Suppressor of inflammatory macrophage apoptosis lncRNA (SIMALR).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Explore the programs pursuing this target and their development progress.

Drug candidates
Developers
Development stage

Clinical trials

Follow the clinical studies evaluating therapies directed at this target.

Trial design
Status
Readouts

Competitive landscape

Compare approaches across drug candidates, modalities, and indications.

Programs
Modalities
Indications

Literature & evidence

Investigate the research and source evidence behind target biology and development.

Publications
Sources
Analysis

Patents

Explore patent activity around therapies and technologies addressing this target.

Patents
Assignees
Technologies

Research & analysis

Connect target biology, drug development, and emerging evidence in your research.

Biology
Development news
Analysis

Bring the full picture into focus.

See how Gosset can support your research on Suppressor of inflammatory macrophage apoptosis lncRNA (SIMALR).

Explore the full profile