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Novel and selective calcitonin-inducing agents

A M Gilbert1, S Caltabiano, D Roberts

  • 1Chemical Sciences, Wyeth-Ayerst Research, 401 North Middletown Road, Pearl River, New York 10965-1299, USA. gilbera@war.wyeth.com

Insights

New xanthine sulfonamides can induce calcitonin (CT) production, offering a potential treatment for osteoporosis and postmenopausal bone loss. These compounds effectively increase CT levels without significant PDE4 inhibition.

Area of Science:

  • Pharmacology
  • Endocrinology
  • Bone Biology

Background:

  • Osteoporosis is a significant health concern, particularly after menopause.
  • Current treatments for bone loss have limitations.
  • Calcitonin (CT) plays a role in bone metabolism.

Purpose of the Study:

  • To identify novel compounds that can induce calcitonin (CT) production.
  • To evaluate the potential of these compounds as a new therapeutic strategy for osteoporosis.

Main Methods:

  • Synthesis and screening of xanthine sulfonamides.
  • Utilized CT-luciferase reporter gene assay (CT-luci) to measure CT transcription.
  • Employed CT secretion/RIA assay (CTS) to assess CT production and release.
  • Evaluated phosphodiesterase type IV (PDE4) inhibitory activity.
  • Assessed bone protection in ovariectomized (OVX) rats using quantitative computed tomography (QCT).

Main Results:

  • Certain di-n-butylxanthine sulfonamides upregulated CT transcription and increased CT production/release.
  • Compound 9 demonstrated a 2.1-fold transcription activation ratio and a 3.6-fold increase in CT secretion.
  • Compound 9 showed significant trabecular bone protection (47-50%) in OVX rats, with minimal PDE4 inhibition (IC50 = 4.1 microM).
  • Efficacy compared favorably to salmon CT in preclinical models.

Conclusions:

  • Xanthine sulfonamides represent a promising class of CT inducers.
  • These compounds offer a potential new therapeutic avenue for treating postmenopausal bone loss and osteoporosis.
  • Compound 9 warrants further investigation as a potential drug candidate.

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