Postmenopausal Osteoporosis

This is a randomized, double-blind, placebo- and active-controlled Phase II study evaluating the efficacy and safety of TST002 injection (a humanized monoclonal antibody) in postmenopausal women with osteoporosis or low bone mass, aged 45-80 years. Approximately 110 participants will be randomized 1:1:1:1:1 (stratified by baseline BMD T-score) to one of five arms: TST002 400 mg every 8 weeks (Q8W), TST002 800 mg Q8W, TST002 1200 mg every 12 weeks (Q12W), placebo, or open-label denosumab 60 mg subcutaneously every 24 weeks. The study includes a screening period (Day -28 to Day -1), a main study period (Week 0-24), and an extension period (Week 25-52), with all participants followed through Week 52 (Day 365). The primary objective is to evaluate the effect of repeated IV TST002 infusions on lumbar spine bone mineral density (BMD). Secondary objectives include characterization of pharmacokinetics, pharmacodynamics, immunogenicity, safety, and tolerability.

This study is a prospective, multicenter, open-label, randomized non-inferiority trial comparing intravenous ibandronate and zoledronic acid as sequential therapy after denosumab discontinuation in postmenopausal women with osteoporosis. This trial primarily targets patients with short-term denosumab exposure (less than three years) and is conducted as a preliminary investigation. The findings are expected to provide foundational evidence to inform the design of future studies assessing sequential therapies following longer-term denosumab treatment.

The goal of this clinical trial is to evaluate the effects of blackcurrant (BC) supplementation on changes in bone density and gut microbiome composition in postmenopausal females.

Osteoporosis is a major cause of morbidity and fragility fractures in postmenopausal women. Bone mineral density (BMD) alone may not fully reflect fracture risk and skeletal fragility. Lumican, an extracellular matrix proteoglycan involved in collagen organization and musculoskeletal tissue homeostasis, has emerged as a potential biomarker for bone health. This prospective observational study aims to investigate the relationship between serum lumican levels, bone mineral density, muscle strength, and clinical fragility indicators in postmenopausal women. Approximately 100 participants will undergo routine osteoporosis assessment including DEXA, laboratory testing, FRAX evaluation, and handgrip strength measurement. The study will evaluate whether serum lumican levels can identify a hidden fragility phenotype beyond conventional bone mineral density measurements.

Osteoporosis is a common condition that increases the risk of bone fractures. Although antiresorptive treatments such as bisphosphonates and denosumab are effective in increasing bone mineral density, some patients continue to experience fractures despite treatment. Advanced glycation end-products (AGEs) accumulate in the body over time and can negatively affect bone quality by altering collagen structure and increasing inflammation. The role of AGE burden in predicting response to osteoporosis treatment has not been fully established. This prospective cohort study aims to evaluate whether baseline AGE burden, measured non-invasively using skin autofluorescence, is associated with treatment response in patients receiving antiresorptive therapy for osteoporosis. Changes in bone mineral density, bone turnover markers, and fracture outcomes will be analyzed in relation to baseline AGE levels. The results of this study may help identify patients at risk for reduced treatment response and residual fracture risk.

Denosumab (Dmab) is a treatment for postmenopausal osteoporosis. However, its withdrawal is associated with a rebound phenomenon associated with an unexpected increased risk of vertebral fractures. Defining the optimal strategy for Dmab withdrawal is critically needed. Investigator propose an open-label randomized superiority strategy trial to compare the 1-year lumbar densitometric efficacy of biomarkers-driven zoledronate (ZOL) infusion vs standardized ZOL treatment to mitigate rebound phenomenon.