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teriparatide (SBL001 / Kauliv / SBL 001)

✓ Approved

Stelis Biopharma · PTH1R

什么是 teriparatide？

teriparatide 是一种治疗药物，由Stelis Biopharma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SBL001, Kauliv, SBL 001
公司Stelis Biopharma
分子靶点PTH1R
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Stelis Biopharma

作用机制

分子靶点

teriparatide 作用于 1 个分子靶点：

PTH1Rparathyroid hormone 1 receptor (PTHR, EKNS)
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

teriparatide 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

相关研究文献

PubMedArchives of osteoporosis2026-09-03

Teriparatide treatment of osteoporosis in solid organ transplant recipients-a single-center experience.

Diker Cohen Talia T, Shraga-Slutzky Ilana I, Kaminer Keren K, Gorshtein Alexander A et al.

Solid organ transplant recipients face high fracture risk with limited evidence guiding anabolic therapy. In this real-world cohort, teriparatide was associated with significant improvements in bone mineral density and acceptable safety without adverse graft effects. These findings support selective anabolic treatment in high-risk transplant recipients and highlight the need for prospective studies. Solid organ transplant (SOT) recipients are at high risk for osteoporosis and fragility fractures due to pre-existing organ dysfunction and long-term immunosuppressive therapy, particularly glucocorticoids. However, evidence supporting the use of anabolic osteoporosis therapy in this population remains limited. We conducted a retrospective cohort study at a large transplant center including adult kidney, lung, and liver transplant recipients selected for teriparatide treatment based on clinical indications for severe post-transplant osteoporosis for at least 3 months. Bone mineral density (BMD), incident fractures, biochemical parameters, renal function, and adverse events were evaluated during treatment and follow-up. Thirty-nine SOT recipients (33% men; mean age 61.3 ± 11.6 years) were included, comprising kidney (n = 10), lung (n = 20), and liver (n = 9) transplant recipients. Prior fragility fractures were present in 90% of patients, and 79% had multiple fractures. Median teriparatide treatment duration was 22.3 months. Significant increases in BMD were observed at the lumbar spine (+11 ± 15%, p = 0.01), femoral neck (+8 ± 14%, p = 0.05), and total hip (+11 ± 16%, p = 0.05). Six patients sustained fractures after teriparatide initiation; only two occurred during active therapy, whereas four occurred after treatment discontinuation. Hypercalcemia occurred in one patient and led to treatment cessation. The estimated glomerular filtration rate declined modestly during the first 6 months and stabilized thereafter; a broadly similar pattern was observed in contemporaneous matched transplant controls. No episodes of graft rejection were observed. In this real-world cohort of SOT recipients with severe osteoporosis, teriparatide therapy was associated with significant improvements in BMD, acceptable safety, and no apparent excess risk to graft function. These findings support the selective use of anabolic therapy in high-risk transplant recipients and highlight the need for prospective studies to define optimal treatment strategies.

PMID 42684545
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PubMedAmerican journal of nephrology2026-08-31

Adynamic Bone Disease in Chronic Kidney Disease: From PTH Suppression-Driven Remodeling Phenotype to Osteoanabolic Therapy.

Lu Kuo-Cheng KC, Hou Yi-Chou YC, Wu Chia-Chao CC, Fang Te-Chao TC et al.

Adynamic bone disease (ABD) is an increasingly prevalent form of low-turnover renal osteodystrophy in advanced chronic kidney disease (CKD). ABD was not recognized as a clinical entity prior to the widespread adoption of PTH-targeted therapeutic strategies, and sustained iatrogenic suppression of parathyroid hormone (PTH) activity is now understood as the primary and defining causal mechanism underlying the adynamic phenotype. Uremic toxins, FGF-23-Klotho dysregulation, impaired vitamin D signaling, chronic inflammation, calcium-phosphate imbalance, and osteocyte-mediated abnormalities function as modulatory contributors that amplify skeletal susceptibility within the context of sustained PTH suppression, rather than independent drivers of ABD. Clinically, ABD is associated with impaired bone quality, increased fracture risk, vascular calcification, and musculoskeletal frailty, abnormalities that are often not adequately reflected by areal bone mineral density measurements alone. ABD in advanced CKD represents a PTH suppression-driven skeletal remodeling phenotype characterized by osteoblast, osteoclast, and osteocyte dysfunction together with disruption of osteoblast-osteoclast coupling. Suppression of Wnt/β-catenin signaling, elevated sclerostin expression, impaired mechanotransduction, skeletal resistance to PTH, and accumulation of uremic toxins collectively contribute to globally reduced remodeling activity and defective microdamage repair. In the context of markedly suppressed bone turnover, antiresorptive therapy is biologically unlikely to confer skeletal benefit and may exacerbate impairment of bone remodeling and renewal. By contrast, anabolic strategies aimed at restoring PTH1R-dependent bone formation and remodeling activation are mechanistically appropriate in CKD-associated ABD. Current evidence suggests that intermittent PTH analog therapy, particularly teriparatide, may improve bone formation markers, bone mineral density, and remodeling activity in selected CKD patients with low-turnover bone disease. Abaloparatide is mechanistically promising but clinically unvalidated in advanced CKD. Romosozumab should not be used in clinical practice for CKD-associated ABD given profound uncertainties regarding cardiovascular safety, vascular calcification, and calcium handling in this population. Practical considerations regarding patient selection, biochemical monitoring, prevention of ABD through avoidance of prolonged PTH suppression, and individualized treatment strategies are also discussed.

PMID 42671953
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PubMedJournal of clinical medicine2026-08-27

Preventing Hip (Proximal Femoral) Fractures: An Evidence-Based Review for Clinicians.

Kawai Toshiyuki T, Okuzu Yaichiro Y, Takaoka Yusuke Y, Natsume Daichi D et al.

Hip fractures are among the most devastating fragility fractures, associated with excess mortality, disability, loss of independence, and substantial healthcare costs. Although age-standardized incidence has declined in several high-income countries, absolute case numbers continue to rise because of population aging. This review summarizes contemporary PubMed-indexed evidence on the epidemiology, risk stratification, and prevention of proximal femoral fractures, with emphasis on hip-fracture outcomes rather than vertebral or composite endpoints alone. We discuss secular trends, FRAX-based case findings and screening, non-pharmacologic strategies, pharmacologic therapy, and health-system interventions relevant to both primary and secondary prevention. Among non-pharmacologic measures, long-term balance-challenging and resistance-based exercise has the most consistent evidence for reducing falls and likely contributes to fracture prevention, whereas multifactorial interventions, home hazard modification, calcium/vitamin D supplementation, and hip protectors are best targeted to selected high-risk populations and care settings. Among medications, bisphosphonates, denosumab, and romosozumab-based sequential strategies show the strongest evidence for reducing hip-fracture risk, while teriparatide and abaloparatide have important roles in very-high-risk patients despite less direct hip-fracture evidence. Menopausal hormone therapy reduces hip fractures in younger postmenopausal women but is limited by extra-skeletal risk, and selective estrogen receptor modulators are primarily vertebral-fracture agents. A major message of this review is that effective prevention depends not only on drug efficacy but also on implementation. Fracture liaison services, orthogeriatric co-management, prompt treatment after fragility fracture, and sustained adherence support are essential to close persistent care gaps. Preventing hip fractures therefore requires an integrated, risk-stratified approach that combines skeletal protection, falls prevention, and reliable health-system delivery.

PMID 42652552
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PubMedClinical therapeutics2026-08-26

Pharmacologic Adjuncts for Bone Stress Injuries in Athletes: A Narrative Review of Current Evidence and Clinical Practice.

Porter Richard R, Rees Jon J

Bone stress injuries (BSIs) are common in athletes, carry substantial time-loss and recurrence risk, and are increasingly managed with bone-active drugs despite a limited evidence base. This narrative review appraises the evidence for pharmacologic adjuncts in BSI, distinguishes the separate clinical indications for which they are proposed, and defines where current evidence does and does not support their use. This is a narrative review; therefore ethical approval was not required. PubMed/MEDLINE, Embase, and the Cochrane Library were searched from inception to June 2026 combining terms for BSI, stress fracture and athletes. Evidence is summarized in an evidence table that states whether each source is directly applicable to BSI in athletes or extrapolated from osteoporosis, traumatic fracture, spinal surgery, military, or animal studies. Greatest weight is given to controlled studies conducted in patients with BSI. Contemporary practice is illustrated by a previously published survey of 126 clinicians working in professional football and by the 2025 international Delphi consensus. The evidence base for treatment options in BSI varies substantially based on the clinical context. Correction of a documented abnormality of energy availability, calcium or protein intake, vitamin D status is a key initial step, but there is no clear evidence that supplementation of replete athletes accelerates healing of an established injury. Evidence for bisphosphonates in BSI is limited to small uncontrolled case series and may even impair bone healing or risk reinjury. Teriparatide data derive predominantly from osteoporotic, fragility fracture, and spinal fusion populations, with a single randomized controlled trial in stress fracture in progress. Newer agents, abaloparatide and romosozumab have no direct evidence in BSI, likely because of their novelty. Across all agents, apparent benefit may represent analgesia and earlier controlled loading rather than accelerated biological healing, given that return-to-play timing is determined by numerous clinical, occupational, and organizational factors. There is currently insufficient evidence to recommend routine use of bisphosphonates or osteoanabolic agents as treatment for an uncomplicated acute BSI in an otherwise healthy athlete. Assessment and correction of nutritional, and metabolic abnormalities, together with load management and rehabilitation, remain the foundation of care. Off-label treatment adjuncts discussed should be considered in recurrent, high-risk or delayed-healing BSI, with shared decision-making focus. Prospective outcome collection is likely to be the most pragmatic way to advance available evidence.

PMID 42648994
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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 USA2026-08-24

Letter of response to "letter of response to 'postpartum timing of teriparatide initiation and BMD response in pregnancy- and lactation-associated osteoporosis: an observational study'".

Lynch Lauren K LK, Shane Elizabeth E, Cohen Adi A

PMID 42635731
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PubMedThe Journal of international medical research2026-08-24

Sequential stress fractures of the ulna and radius in a patient with neurofibromatosis type 1: A case report.

Kang Hyun Tak HT, Jin Woong Geun WG, Kang Hong Je HJ

Stress fractures of the forearm are uncommon, and to our knowledge, sequential involvement of both the ulna and radius has not been well characterized. Neurofibromatosis type 1 is associated with increased bone fragility and delayed fracture healing due to impaired osteoblastic differentiation, reduced mineralization capacity, and increased osteoclastic activity. We report the case of a woman in her early 60s with neurofibromatosis type 1 and lower-extremity weakness who relied on upper-extremity weight-bearing ambulation. She initially developed a nondisplaced transverse stress fracture of the proximal ulnar shaft with delayed union, which subsequently achieved union following conservative treatment, including teriparatide. Approximately 24 months after the initial ulnar fracture, she developed a new nondisplaced stress fracture of the radial shaft, suggestive of a possible stress-transfer phenomenon related to altered load distribution across the forearm. Repeated conservative treatment with strict weight-bearing restriction resulted in radiographic union with restoration of functional forearm motion. This case highlights the importance of recognizing altered forearm load distribution to reduce the risk of secondary stress injury.

PMID 42635746
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