Evidence map›Paper›PMID 40524167›Full record

ArticleJournal of biomedical science2025

Targeting neuroinflammation: 3-monothiopomalidomide a new drug candidate to mitigate traumatic brain injury and neurodegeneration.

Shih Chang Hsueh, Pathik Parekh, Buyandelger Batsaikhan, Neil Vargesson, David Tweedie, Weiming Luo, Chirag N Patel, Dong Liu, Ross A McDevitt, Abdul Mannan Baig and 10 more

Abstract read
In one paragraph

Article in Journal of biomedical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Targeting neuroinflammation to enhance recovery after brain injury.Annals of medicine and surgery (2012) · 2026
    Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Shih Chang Hsueh *Drug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Pathik Parekh *Drug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Buyandelger BatsaikhanDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Neil VargessonSchool of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Aberdeen, AB25 2ZD, Scotland, UK.
David TweedieDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Weiming LuoDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Chirag N PatelDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Dong LiuDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA.
Ross A McDevittComparative Medicine Section, National Institute on Aging, Baltimore, MD, USA.
Abdul Mannan BaigSt. George Hospital, 83043, Bad Aibling, Germany.
Yu Kyung KimAevis Bio Inc., Daejeon, 34141, Republic of Korea.
Sun KimAevis Bio Inc., Daejeon, 34141, Republic of Korea.
Inho HwangAevis Bio Inc., Daejeon, 34141, Republic of Korea.
Juwan KimAevis Bio Inc., Daejeon, 34141, Republic of Korea.
Mee Youn LeeAevis Bio Inc., Daejeon, 34141, Republic of Korea.
Anna R CartaDepartment of Biomedical Sciences, University of Cagliari, Cagliari, Italy.
Warren R SelmanThe Marcus Neuroscience Institute, Baptist Health South Florida, Boca Raton, USA.
Barry J HofferHoffer Consulting, Cleveland, OH, 44124, USA.
Dong Seok KimAevis Bio Inc., Daejeon, 34141, Republic of Korea.
Nigel H GreigDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program National Institute on Aging, NIH, Baltimore, MD, 21224, USA. Greign@grc.nia.nih.gov.ORCID http://orcid.org/0000-0002-3032-1468

Funding

Eating Behaviors in Homebound Older AdultsK01AG000994 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LOCHER, JULIE L · 2001 to 2005
$503k
Korea Drug Development Fund funded by the Ministry of Science and ICT, Ministry of Trade, Industry, and Energy, and Ministry of Health and Welfare, Republic of Korea KDDF RS-2024-00338017Ministry of Health & Welfare and Ministry of Science and ICT, Republic of Korea RS-2024-0034124913NIA NIH HHS AG000994NIA NIH HHS K01 AG000994
6 · The paper itself

Abstract

backgroundTraumatic Brain Injury (TBI) is a major risk factor for neurodegenerative disorders such as Parkinson's disease (PD) and Alzheimer's disease (AD), with neuroinflammation playing a critical role in the secondary cell death that exacerbates the initial injury. While targeting neuroinflammation holds significant therapeutic promise, clinical trials of available anti-inflammatory agents have fallen short. 3-Mono-thiopomalidomide (3-MP), a novel immunomodulatory imide drug (IMiD), was designed to curb inflammation without the adverse effects of traditional IMiDs and was evaluated across models involving neuroinflammation.

methods3-MP anti-inflammatory activity was evaluated across cellular (RAW 264.7, IMG cells) and mouse studies following lipopolysaccharide (LPS)-challenge (for pro- and anti-inflammatory cytokines/chemokines), and mice subjected to controlled cortical impact (CCI) moderate traumatic brain injury (TBI). 3-MP human cereblon binding, including neosubstrate and molecular modeling evaluation, as well as chicken teratogenicity, ex vivo mouse and human stability studies, and mouse pharmacokinetics were appraised.

results3-MP binds human cereblon, a key protein in the E3 ubiquitin ligase complex, without triggering downstream cascades leading to thalidomide-like teratogenicity in chicken embryos. 3-MP reduces pro-inflammatory markers in LPS-stimulated mouse macrophage and microglial cell cultures, and lowers pro-inflammatory cytokine/chemokine levels in plasma and brain of mice challenged with systemic LPS without lowering anti-inflammatory IL-10. 3-MP readily enters brain following systemic administration, and achieves a brain/plasma concentration ratio of 0.44-0.47. 3-MP mitigates behavioral impairments and reduces activation of astrocytes and microglia in mice challenged with CCI TBI.

conclusion3-MP represents a promising new class of thalidomide-like IMiDs with potent anti-inflammatory effects that offers potential for treating TBI and possibly other neurodegenerative diseases possessing a prominent neuroinflammatory component.

Indexed as

Anti-Inflammatory AgentsBrain Injuries, TraumaticNeurodegenerative DiseasesNeuroinflammatory DiseasesThalidomideAnimalsChick EmbryoHumansMaleMiceMice, Inbred C57BLRAW 264.7 CellsAnti-Inflammatory AgentsThalidomideCereblonImmunomodulatory imide drugs (IMiDs)MicrogliaNeurodegenerationNeuroinflammationPomalidomideSpalt like transcription factor 4 (SALL4)TeratogenicityTraumatic brain injury

Identifiers

PMID40524167
PMCPMC12172326

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.