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Related Concept Videos

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Related Experiment Video

Updated: Jan 6, 2026

A Simple and Efficient Method for Testing Immunomodulatory Agents for Generation of Tolerogenic Dendritic Cells from Human CD14+ Monocytes
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LPX-TI641, a Tim3/4 Agonist, Induces Long-Term Immune Tolerance in Multiple Sclerosis Models.

Anas M Fathallah1, Abdulraouf Ramadan1, Basel Karzoun1

  • 1LAPIX Therapeutics Inc., Cambridge, MA 021141, USA.

Pharmaceutics
|November 27, 2025
PubMed
Summary
This summary is machine-generated.

A novel drug, LPX-TI641, shows promise for multiple sclerosis (MS) by expanding regulatory T cells (Tregs) to restore immune tolerance. This antigen-independent approach offers a potential new treatment for MS, overcoming limitations of current therapies.

Keywords:
Regulatory T-cells (Tregs)drug discoveryimmune regulationimmune tolerancemultiple sclerosisoral therapy

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Area of Science:

  • Immunology
  • Neuroscience
  • Pharmacology

Background:

  • Current multiple sclerosis (MS) treatments face safety and tolerability issues.
  • Antigen-specific therapies for MS are limited by the need for known autoantigens.
  • LPX-TI641 is a novel, orally available small-molecule agonist of Tim-3/4, offering an antigen-independent strategy to restore immune tolerance via regulatory T cell (Treg) expansion.

Purpose of the Study:

  • To evaluate LPX-TI641's ability to induce Treg populations in vitro.
  • To assess the therapeutic efficacy of LPX-TI641 in experimental autoimmune encephalomyelitis (EAE) mouse models.
  • To analyze Treg phenotype and function in response to LPX-TI641 in peripheral blood mononuclear cells (PBMCs) from people with MS (PwMS).

Main Methods:

  • In vitro induction of Treg populations using murine splenocytes.
  • In vivo efficacy assessment in MOG35-55- and PLP139-151-induced EAE mouse models.
  • Ex vivo analysis of PBMCs from PwMS for Treg response to LPX-TI641.

Main Results:

  • LPX-TI641 demonstrated dose-dependent expansion of CD4+Foxp3+ and CD4+Foxp3+Tim-3+ Tregs in vitro.
  • In EAE models, LPX-TI641 significantly reduced disease severity, prevented relapses, and maintained clinical benefit post-treatment.
  • LPX-TI641 restored diminished Tim-3+ Treg populations and reversed Treg dysfunction in PBMCs from PwMS.
  • Therapeutic efficacy in animal models was comparable to or surpassed natalizumab.

Conclusions:

  • LPX-TI641 promotes antigen-independent immune tolerance by activating Tim receptors and expanding Tregs.
  • These findings suggest LPX-TI641 as a potential novel therapeutic candidate for MS.
  • LPX-TI641 may address limitations associated with current disease-modifying therapies for MS.