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denosumab (RTPR045 / RTPR 045 / DenosteRel)

✓ Approved

Reliance Life Sciences Private Limited · TNFSF11 · 单克隆抗体

什么是 denosumab？

denosumab 是一种单克隆抗体，由Reliance Life Sciences Private Limited研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Subcutaneous Injection。

药物档案

商品名RTPR045, RTPR 045, DenosteRel
公司Reliance Life Sciences Private Limited
药物类别单克隆抗体, 抗体
分子靶点TNFSF11
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Reliance Life Sciences Private Limited

作用机制

分子靶点

denosumab 作用于 1 个分子靶点：

TNFSF11TNF superfamily member 11 (ODF, CD254)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

denosumab 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Bone cancer✓ Approved
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

相关研究文献

PubMedJournal of clinical densitometry : the official journal of the International Society for Clinical Densitometry2026-08-04

Sequential therapy following romosozumab: real-world comparison of denosumab and bisphosphonates with 2-year follow-up.

Nakano Ryo R, Ichisawa Ayumi A, Saruta Kenya K, Kogawa Masakazu M et al.

Sequential therapy is required to maintain bone mineral density (BMD) gains after romosozumab treatment; however, the optimal sequential therapy remains unclear. This study compared denosumab with bisphosphonates as sequential therapy following romosozumab treatment in real-world practice. This retrospective observational study analyzed 315 patients with osteoporosis who received 12 months of romosozumab at Mutsu General Hospital (April 2019-April 2024) with a minimum 12-month follow-up. Sequential therapy was chosen by the physician and patient after consideration of renal function, gastrointestinal tolerance, adherence, and patient preference. The total enrollment was 315 patients: denosumab plus vitamin D (n = 158), bisphosphonates plus vitamin D (n = 95), no sequential therapy (n = 13), or other regimens (n = 49). For BMD analysis, 12-month data were available for 264 patients (denosumab n = 157, bisphosphonates n = 95, no sequential n = 12). The primary outcomes were BMD changes at the lumbar spine and total hip. Sequential therapy was implemented in 92.7% of the patients. At 12 months, both the denosumab and bisphosphonate groups showed significant BMD increases, with no statistical difference (lumbar spine: +12.8% vs. +13.6%, p = 0.565; total hip: +3.8% vs. +4.0%, p = 0.926). At 24 months, denosumab showed greater continued increases (lumbar spine: +5.9% vs. +2.2%; total hip: +5.8% vs. +4.0%). Patients without sequential therapy experienced a BMD decline from year 1 to 2 (lumbar spine: -5.4%). TRACP-5b (a bone resorption marker) decreased by approximately 30% in both sequential therapy groups (medians: denosumab -30.3%, bisphosphonates -30.6%). Incident fracture rates were similar between denosumab (6.3%) and bisphosphonates (6.3%) but numerically higher in the group without sequential therapy (15.4%). Sequential therapy following romosozumab administration is essential for preventing BMD loss and reducing fracture risk. Both denosumab and bisphosphonates were effective, with denosumab showing superior sustained BMD gains in the second year.

PMID 42546512
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PubMedInternational immunopharmacology2026-08-04

Advances in the study of the role of bone immunity in physiological and pathological processes related to bone metabolism.

Jin Zhuoru Z, Liu Lisheng L, Wang Heran H, Wei Yufei Y et al.

Bone metabolism is regulated by immune cells that maintain skeletal homeostasis through cytokine secretion and cell interactions. Disruption of this regulation-by inflammation, autoimmunity, or aging-drives pathological bone diseases including osteoporosis and rheumatoid arthritis. Single-cell technologies and exosome biology have revealed previously unrecognized immune subsets and regulatory layers within the bone microenvironment. Osteoimmunology has elucidated the interplay between macrophages, T cells, B cells, NK cells, neutrophils, dendritic cells, and mast cells in bone remodeling. These cells form dynamic interaction networks-Treg-M2 feedback loops, Th17-neutrophil amplification, and B-T-osteoclast axes-that collectively determine net skeletal outcome. Immune cells regulate osteoclast and osteoblast function through TNF-α, IL-6, IL-17 A, and RANKL, with highly context-dependent effects. Immunosenescence has emerged as a key driver of age-related bone loss. The RANKL/RANK/OPG axis serves as the central signaling hub, modulated by Sema3A/Wnt/β-catenin, PI3K/Akt, JAK/STAT, and Notch. Dysregulation of these pathways underlies osteoporosis, RA, intervertebral disc degeneration, ankylosing spondylitis, and cancer bone metastasis. Clinically, denosumab and cytokine-targeted biologics (anti-TNF-α, anti-IL-6R, anti-IL-17 A) demonstrate bone-protective effects, while bispecific antibodies, CAR-Treg cells, and senolytics represent emerging strategies. The net skeletal effect of the immune system is determined by the balance of interacting cell types, cytokine networks, and signaling pathways. Future progress requires single-cell spatiotemporal multi-omics, cell-type-specific immunotherapies, elucidation of the gut-bone axis, and systematic evaluation of combination strategies pairing immunomodulators with anti-resorptives, anabolic agents, or senolytics.

PMID 42546515
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PubMedJournal of investigative medicine high impact case reports2026-08-03

Suspected Denosumab-Associated Acute Coronary Syndrome.

Maharaj Matthew M, Katwaroo Arun A, Ramcharan Priya P, Frederick Jean-Marie JM et al.

Denosumab, a monoclonal antibody (mAb) targeting receptor activator of nuclear factor-κB ligand (RANKL), is commonly used in managing metabolic bone diseases and giant cell tumors (GCTs) of bone. Growing evidence suggests that RANKL inhibition may influence cardiovascular health by impacting endothelial function, inflammatory pathways, vascular smooth muscle cell behavior, and systemic calcium regulation. We report a case of a 48-year-old Caribbean-South Asian man with recurrent GCTs who received three subcutaneous doses of denosumab and soon thereafter developed an anterior ST-elevation acute coronary syndrome (STE-ACS). The patient had no traditional cardiometabolic risk factors. Coronary angiography revealed thrombotic occlusion of the proximal left anterior descending artery (LAD), which was successfully treated with primary percutaneous coronary intervention (PPCI) and guideline-directed medical therapy (GDMT). Given the lack of modifiable risk factors, a significant family history, and biologically plausible mechanisms linking RANKL inhibition to atherothrombotic events, a denosumab-associated myocardial infarction was considered the most probable cause.

PMID 42544531
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PubMedFrontiers in dental medicine2026-08-02

Periodontal disease and endocrine imbalance: a molecular pathways perspective.

Martínez-García Mireya M, Hernández-Lemus Enrique E

Periodontitis is a chronic multifactorial inflammatory disease whose pathological consequences extend well beyond the oral cavity to affect systemic health through the dissemination of pro-inflammatory mediators, bacteremic episodes, and the amplification of low-grade systemic inflammation. Concurrently, the endocrine system functions as a central regulator of periodontal tissue homeostasis, with hormone receptors for estrogens, androgens, glucocorticoids, insulin, thyroid hormones, and vitamin D expressed across the principal cell populations of the periodontium, including gingival fibroblasts, PDL cells, osteoblasts, osteoclasts, and epithelial cells. This narrative review synthesizes current evidence on the molecular pathways mediating the bidirectional relationship between periodontal disease and endocrine imbalance, integrating experimental, clinical, and systems-level bioinformatics data to provide a comprehensive mechanistic framework for this interaction. We examine how estrogen deficiency, progesterone excess, androgen dysregulation, insulin resistance, adipokine imbalance, thyroid dysfunction, glucocorticoid excess or deficiency, and perturbations of the parathyroid hormone and vitamin D axes each contribute to periodontal susceptibility through distinct but convergent molecular mechanisms involving NF- κ B activation, NLRP3 inflammasome-driven IL-1 β and IL-18 maturation, cytokine network dysregulation, oxidative stress amplification, and disruption of the RANKL/OPG balance governing alveolar bone homeostasis. We also discuss key hub genes including TNF, IL6, LEP, NOS3, STAT3, and VEGFA as molecular nodes that simultaneously participate in endocrine and periodontal signaling, and we highlight the PI3K/Akt, AGE-RAGE, JAK-STAT, Th17 differentiation, and HIF-1 pathways as the most significantly enriched molecular routes of endocrine-periodontal crosstalk. The RANKL/OPG axis emerges as a central integrator of hormonal and inflammatory inputs to alveolar bone metabolism, with estrogen, PTH, glucocorticoids, vitamin D, leptin, and adiponectin each converging on this molecular switch through receptor-mediated mechanisms that are additive to the inflammatory RANKL upregulation driven by IL-1 β , IL-6, IL-17, and TNF- α in active periodontal lesions. Emerging pharmacological agents at the endocrine-periodontal interface, including GLP-1 receptor agonists, denosumab, statins, vitamin D supplementation, and specialized pro-resolving mediators, offer mechanistically grounded opportunities for integrated therapeutic strategies that address both oral and systemic disease simultaneously. The diagnostic and therapeutic implications of these molecular relationships demand a fundamental reorientation of clinical management toward interdisciplinary models in which periodontal assessment is incorporated into the evaluation of patients with endocrine disorders, endocrine status is systematically characterized in patients with severe or treatment-refractory periodontitis, and therapeutic decisions in both specialties are made with explicit awareness of the shared molecular architecture linking them.

PMID 42539866
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PubMedOsteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA2026-07-31

The cost-effectiveness of biosimilar denosumab in postmenopausal osteoporosis: implications of baseline fracture risk and drug price.

Li Edward E, Mirzayeh Fashami Fatemeh F, Kane Sarah S, McTavish Rebecca R et al.

Biosimilar denosumab is a dominant treatment strategy (i.e., more effective and less costly) across varying levels of baseline fracture risk with sufficient price reductions. Given its superior efficacy and safety, it may be considered a first-line therapy for the treatment of women with postmenopausal osteoporosis at high risk of fracture in the United States (US). Large-scale adoption of biosimilar denosumab as a first-line therapy in this population is anticipated to lead to health improvements at a lower overall cost. Postmenopausal osteoporosis (PMO) remains undertreated in the US. According to clinical practice guidelines, bisphosphonates and denosumab are recommended therapies for women at high risk of fracture, but bisphosphonates have been preferred due to lower cost. The introduction of biosimilar denosumab may reduce prices and improve access. This study evaluates the cost-effectiveness of biosimilar denosumab compared to bisphosphonates and no intervention in women with PMO in the US across different baseline fracture risks and biosimilar denosumab pricing scenarios. A validated Markov cohort model estimated cost-effectiveness of biosimilar denosumab versus alendronate, risedronate, ibandronate, zoledronic acid, and no intervention. Patients were stratified into four risk categories based on T-score and prior vertebral fracture. The analyses explored the impact of changes in baseline fracture risk and biosimilar denosumab pricing. The cost-effectiveness of biosimilar denosumab improved with increasing fracture risk (categories 1-4 represent increasing risk). Biosimilar denosumab was dominant (i.e., more effective and less costly) when priced at $120-$180, $376-$451, $376-$481, and $857-$1188 for risk categories 1, 2, 3, and 4, respectively. At a 75% price reduction (i.e., $376), biosimilar denosumab was dominant versus all comparators for risk categories 2, 3, and 4. With sufficient price reductions, biosimilar denosumab is a dominant strategy across varying levels of baseline fracture risk. Biosimilar denosumab's superior efficacy and favorable safety profile compared to bisphosphonates, along with anticipated price declines, support its potential as a first-line therapy for women with PMO at high-risk of fracture in the US.

PMID 42533098
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PubMedZhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology2026-07-31

[Advances in the diagnosis and treatment of diffuse sclerosing osteomyelitis of the jaw].

Zhang G Q GQ, An J G JG

Diffuse sclerosing osteomyelitis of the jaw (DSO) is a rare non-suppurative inflammatory bone disease of unknown etiology, characterized by a chronic course, recurrent pain, and diffuse jawbone sclerosis. Diagnosis is challenging, and conventional surgical and anti-infective therapies have limited efficacy with high recurrence. Recent studies reveal that DSO is closely associated with synovitis-acne-pustulosis-hyperostosis-osteitis syndrome. The core mechanisms involves autoinflammatory bone-immune imbalance, particularly dysregulation of the RANKL/RANK/OPG signaling pathway. Consequently, the treatment strategy for DSO has fundamentally shifted from surgery and anti-infective drugs to a precision medicine approach with bisphosphonates, as the cornerstone,and expanded to include denosumab, tumor necrosis factor-α inhibitors, and JAK inhibitors. This article systematically reviews the etiology, diagnosis, key differential diagnoses, and recent advances in pharmacotherapy, and proposes a stepped treatment algorithm.

PMID 42532526
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