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BP-1-102 inhibits multiple pathways of NFATc1 activation to alleviate osteoporosis and downregulate osteoclast

Jihao Yang1, Li Chen2, Guoli Gan3

  • 1Department of Emergency Surgery, The First Affiliated Hospital of Zhengzhou University, Henan Medical Key Laboratory of Emergency and Trauma Research, Zhengzhou, Henan, 450052, China.

Biochemical and Biophysical Research Communications
|June 17, 2026
PubMed

Insights

The STAT3 inhibitor BP-1-102 effectively prevents osteoclast formation and bone loss in osteoporosis models. This compound targets key signaling pathways, showing therapeutic potential for bone diseases.

Area of Science:

  • Bone Biology
  • Cell Signaling
  • Pharmacology

Background:

  • Signal transducer and activator of transcription 3 (STAT3) promotes osteoclastogenesis by activating nuclear factor of activated T cells 1 (NFATc1).
  • Osteoclast differentiation is crucial in bone remodeling and diseases like osteoporosis.

Purpose of the Study:

  • To investigate the efficacy of the STAT3 inhibitor BP-1-102 in suppressing RANKL-induced osteoclast differentiation.
  • To elucidate the molecular mechanisms underlying BP-1-102's effects on osteoclastogenesis and bone loss.

Main Methods:

  • In vitro studies using bone marrow macrophages (BMMs) treated with RANKL and BP-1-102.
  • Gene expression analysis, Western blotting for protein phosphorylation, and cell viability assays.
  • In vivo studies using an ovariectomized mouse model to assess bone loss and osteoclast activity.

Main Results:

  • BP-1-102 (2.5/5 μM) suppressed osteoclast formation and specific gene expression without cytotoxicity.
  • BP-1-102 inhibited STAT3 phosphorylation and NFATc1 expression, downregulating the c-Fos/NFATc1 axis via MAPK and NF-κB pathways.
  • In vivo, BP-1-102 attenuated bone loss in ovariectomized mice, reducing osteoclast numbers and inhibiting STAT3/p38 phosphorylation.

Conclusions:

  • BP-1-102 demonstrates significant therapeutic potential for osteoporosis by inhibiting osteoclastogenesis.
  • The compound effectively rescues bone loss by targeting the p-STAT3/MAPK/NF-κB signaling cascade.
Keywords:
BP-1-102Mitogen-activated protein kinaseOsteoclastsOsteoporosisOvariectomySignal transducer and activator of transcription 3

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