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Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...

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Related Experiment Video

Updated: Jul 11, 2026

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
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ART26.12, an FABP5 Inhibitor, Shows Efficacy in Preclinical Psoriasis Models.

William G Warren1, Myles Osborn1, Andrew Yates1

  • 1Artelo Biosciences, Cheshire, United Kingdom.

The Journal of Investigative Dermatology
|April 10, 2025
PubMed
Summary

The fatty acid-binding protein 5 (FABP5) inhibitor ART26.12 shows promise for treating psoriasis. In preclinical models, ART26.12 reduced key disease markers and improved skin pathology, suggesting its potential as an oral therapy.

Keywords:
AntipsoriaticFABP5ImiquimodInflammation

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Area of Science:

  • Dermatology
  • Pharmacology
  • Molecular Biology

Background:

  • Fatty acid-binding protein 5 (FABP5) is implicated in the pathogenesis of psoriasis.
  • Developing targeted therapies for psoriasis is crucial due to its chronic inflammatory nature.

Purpose of the Study:

  • To evaluate the efficacy of ART26.12, a selective FABP5 inhibitor, in preclinical models of psoriasis.
  • To investigate the molecular mechanisms underlying ART26.12's therapeutic effects.

Main Methods:

  • In vitro studies utilized cytokine-stimulated human epidermis treated with ART26.12 or a JAK1 inhibitor, followed by gene expression analysis.
  • In vivo studies employed the imiquimod-induced mouse model of psoriasis, with oral administration of ART26.12 or a TYK2 inhibitor (BMS-986165).
  • Histopathological, proteomic, and lipidomic analyses were performed to assess treatment effects.

Main Results:

  • ART26.12 reduced psoriasis-related gene expression, including cytokines and markers of keratinocyte proliferation, in vitro.
  • In vivo, ART26.12 demonstrated comparable efficacy to BMS-986165 in reducing psoriasis-like symptoms and improving histopathological features.
  • Proteomic and lipidomic analyses revealed that ART26.12 modulated key signaling pathways (PPAR, NF-kB, PKC) and lipid metabolism, including ceramides.

Conclusions:

  • ART26.12 exhibits significant therapeutic potential as an orally active agent for psoriasis.
  • The mechanism of action involves modulation of lipid metabolism and downstream inflammatory and differentiation pathways.
  • Further clinical investigation of ART26.12 for psoriasis treatment is warranted.