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Related Experiment Video

Updated: Jul 5, 2025

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An ADAM10 Exosite Inhibitor Is Efficacious in an In Vivo Collagen-Induced Arthritis Model.

Juan Diez1, Michael E Selsted2, Thomas D Bannister3

  • 1Department of Pharmaceutical Sciences, Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, 3321 College Avenue, Fort Lauderdale, FL 33314, USA.

Pharmaceuticals (Basel, Switzerland)
|January 23, 2024
PubMed
Summary
This summary is machine-generated.

A novel drug, CID3117694, shows promise for rheumatoid arthritis (RA) treatment by inhibiting ADAM10. This compound effectively reduced RA symptoms and inflammation in mice with minimal toxicity, suggesting a new therapeutic avenue.

Keywords:
ADAM10collagen-induced arthritisexosite inhibitorin vivo efficacyrheumatoid arthritis

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Area of Science:

  • Immunology
  • Pharmacology
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) is a widespread autoimmune disease impacting millions globally.
  • Current disease-modifying anti-rheumatic drugs (DMARDs) have limited efficacy for many RA patients.
  • ADAM10 (a disintegrin and metalloproteinase 10) is implicated in inflammatory factor release, presenting a potential therapeutic target for RA.

Purpose of the Study:

  • To evaluate the pharmacokinetic properties and in vivo efficacy of CID3117694, a novel non-zinc-binding inhibitor targeting ADAM10.
  • To assess the therapeutic potential of inhibiting ADAM10 exosite in a preclinical model of rheumatoid arthritis.

Main Methods:

  • Pharmacokinetic analysis of CID3117694 after oral administration in mice.
  • Assessment of CID3117694 efficacy in the collagen-induced arthritis (CIA) mouse model.
  • Dose-dependent administration of CID3117694 (10, 30, 50 mg/kg/day) for 28 days, monitoring disease score, RA markers, and joint pathology.

Main Results:

  • CID3117694 demonstrated oral bioavailability in blood and synovial fluid.
  • The compound significantly and dose-dependently improved disease scores in CIA mice.
  • CID3117694 reduced RA markers, inflammation, hyperplasia, pannus formation, and cartilage erosion.
  • No clinical signs of distress were observed, indicating low toxicity of CID3117694.

Conclusions:

  • Inhibition of ADAM10 exosite by CID3117694 is a promising therapeutic strategy for rheumatoid arthritis.
  • CID3117694 exhibits favorable pharmacokinetics and potent anti-arthritic effects in vivo.
  • The findings support further development of ADAM10 inhibitors for RA treatment.