The goal of this clinical trial is to determine the change in VBQ score, T score, TBS, and Hounsfield Units (HU) after 3-6 months of treatment with abaloparatide in osteoporotic patients who will undergo spinal fusion and decompression for lumbar degenerative disease. The main question[s] it aims to answer is:
Does abaloparatide improve bone density in these patients, as defined by VBQ score compared to traditional methods such as DEXA and Hounsfield Units Does abaloparatide reduce the incidence of postoperative mechanical complications, including adjacent segment disease, subsidence, and proximal junctional kyphosis (PKJ)?
Participants will undergo a presurgical assessments and trained in clinic on the subcutaneous application of abaloparatide. Prior to treatment, patients will have baseline assessments, including a lumbar MRI, DEXA scan, and lumbar CT. Post-surgically, participants will administer abaloparatide and return to clinic after 3-6 months for follow-up assessments including a new MRI, lumbar CT, and DEXA scan. Patients will be followed for up to 2 years postoperatively to identify complications such as adjacent segment disease, pseudarthrosis, failure of instrumentation, and PJK.

开始日期2026-06-18

申办/合作机构

State University of New York at Buffalo

JPRN-jRCT2031250561

/ RecruitingN/A

Cohort Study using EBM Provider for Evaluation of the Risk of Cardiovascular Events associated with Abaloparatide versus with Teriparatide in Patients with Osteoporosis

开始日期2025-09-11

申办/合作机构

Teijin Pharma Ltd.

NCT06898060

/ Not yet recruiting临床3期

A Multicenter, Randomized, Open-label, Parallel Controlled, Phase III Clinical Study to Evaluate the Efficacy and Safety of Abaloparatide Injection (QLG2128) in the Treatment of Postmenopausal Women With Osteoporosis and at High Risk of Fracture

The purpose of this study is to evaluate the efficacy and safety of QLG2128 in the treatment of postmenopausal women with osteoporosis and at high risk of fracture.

开始日期2025-06-01

申办/合作机构

齐鲁制药有限公司

100 项与阿巴帕肽相关的临床结果

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100 项与阿巴帕肽相关的转化医学

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100 项与阿巴帕肽相关的专利（医药）

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376

项与阿巴帕肽相关的文献（医药）

2026-11-01·BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY

Bone Anabolic Treatment in Patients With Chronic Kidney Disease: A Systematic Review

Review

作者: Hauge, Sabina Chaudhary ; Hansen, Ditte ; Kafa, Huriye Seyma

ABSTRACT:

Background:

Chronic kidney disease (CKD) associated osteoporosis leads to an increased risk of bone fracture in patients with CKD. Evidence on the efficacy and safety of anti‐osteoporotic medications is limited for this group. This systematic review aimed to examine the efficacy and safety of anabolic parathyroid hormone (PTH) treatment in patients with CKD Stages 4–5D.

Methods:

MEDLINE, EMBASE and ClinicalTrials.gov were searched systematically for randomized controlled trials (RCTs) investigating teriparatide, natpara, or abaloparatide in adult patients with CKD Stages 4–5D, including kidney transplant recipients. The primary outcome was the change in bone mineral density (BMD) during follow‐up measured at the lumbar spine (LS), femoral neck (FN) and total hip (TH). The secondary outcomes included bone turnover markers, fractures, histomorphometric results from bone biopsies and adverse events (AEs).

Results:

Two RCTs were included. A subgroup analysis of patients with CKD Stage 4 ( n = 5) showed that teriparatide improved BMD at the LS and FN. Another trial ( n = 61) in CKD Stage 5D showed significant BMD improvement at the TH compared to the control group. AEs were observed with higher frequency in the teriparatide‐treated group.

Conclusion:

Treatment with teriparatide seems to improve BMD in patients with CKD Stages 4–5D, but evidence on efficacy and safety is limited.

Trial Registration:

PROSPERO: CRD42024527086

2026-10-01·Journal of Oral Biosciences

Pharmacological effects of PTH1R agonists on jaw bone fracture, periodontitis, orthodontic treatment and MRONJ: a view from dosing regimen settings

Review

作者: Iimura, Tadahiro ; Tsuji, Naoki ; Nakanishi-Kimura, Atsuko ; Scheller, Erica L

BACKGROUND:

Parathyroid hormone (PTH) and PTH-related peptide (PTHrP) are endogenous ligands of PTH type I receptor (PTH1R), which are essential for skeletal development and homeostasis. Since the intermittent application of these molecules to organisms exerts bone anabolic effects, they are used pharmacologically to increase bone mass and stimulate bone formation. Teriparatide, an N-terminal 34 amino acid fragment of human PTH, and abaloparatide, a derivative of the N-terminal 34 amino acid of human PTHrP, have been pharmaceutically developed and clinically applied to treat severe osteoporosis and are categorized as PTH1R agonists. An increasing number of clinical and preclinical studies have demonstrated that PTH1R agonists can be used in dental medicine, including jaw bone regeneration and orthodontic treatment, periodontitis, and the management of medication-related osteonecrosis of the jaw (MRONJ). However, it is unclear whether the mandibular bone responds pharmacologically to PTH1R agonists in the same way as other trunk bones, such as the limb and axial bones.

HIGHLIGHT:

Compared with studies using long and vertebral bones, the beneficial effects of PTH1R agonists on the mandibular bone appear to require higher doses and longer treatment durations.

CONCLUSION:

Clinical application of PTH1R agonists in dental medicine may result in promising outcomes. However, dosing regimens and the timing of their application should be further investigated with knowledge of the biological uniqueness of the mandibular bone.

2026-10-01·CLINICAL THERAPEUTICS

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

Review

作者: Porter, Richard ; Rees, Jon

PURPOSE:

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.

METHODS:

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.

FINDINGS:

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.

IMPLICATIONS:

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.

137

项与阿巴帕肽相关的新闻（医药）

2026-10-23

·IVday Bio

甲状旁腺激素受体信号通路、骨细胞与糖尿病诱导骨病变

PTH receptor signaling, osteocytes, and diabetes-induced bone disease Silvia Marino, …, and Teresita Bellido Department of Physiology and Cell Biology, University of Arkansas for Medical Sciences, Little Rock, AR, USA. ---Nat Rec Endocrinol. 2024. doi:10.1038/s41574-024-01014-7. 摘要：甲状旁腺激素1型受体（Parathyroid Hormone 1 Receptor, PTH1R）是B类G蛋白偶联受体（GPCR）家族的重要成员，广泛分布于骨骼、肾脏、大脑、心脏等多种组织中。作为钙磷稳态和骨代谢的核心调控因子，PTH1R通过与甲状旁腺激素（PTH）和甲状旁腺激素相关肽（PTHrP）结合，激活下游多条信号通路（如Gs/cAMP/PKA、Gq/PLC/PKC等），参与胚胎发育、钙磷代谢、肿瘤进展及多种疾病的病理生理过程。其功能异常与骨质疏松症、甲状旁腺功能减退症、原发性牙齿萌出障碍（PFE）等疾病密切相关，是当前药物研发的重要靶点。PTH1R是骨代谢的核心调控开关。其间歇性激活通过促进成骨细胞活性和抑制骨硬化蛋白，主导骨形成并轻度调节骨吸收，从而增加骨量，对抗骨质疏松；而其持续性激活则通过显著上调RANKL/OPG比值，强烈刺激破骨细胞骨吸收，导致骨量丢失，引发或加剧骨质疏松。这种信号持续时间的差异决定了其对骨平衡的最终效应。因此，PTH1R是理解骨代谢平衡、骨质疏松发病机制以及开发相关靶向治疗药物的核心分子。 PTH1R通路：从配体到基因天然（PTH 和 PTHrP）或合成（ABL）配体与成骨细胞谱系细胞上的 PTH1R 结合，会激活 G 蛋白（Gαβγ），随后启动细胞内信号通路。PTH1R/Gαs 信号通路会激活腺苷酸环化酶（AC），累积 cAMP，激活蛋白激酶 A（PKA），并抑制盐诱导激酶（SIK2/3）。SIK 活性被抑制后，会导致 IIa 类组蛋白去乙酰化酶（HDAC4/5）和 CREB 调控的转录共激活因子（CRTC2）去磷酸化。随后它们进入细胞核，HDAC4/5/Medf2C 依赖的 SOST 基因表达下降，而 CRTC2/CREB 依赖的 RANKL 基因表达上升。除了这些，还有其他依赖或不依赖 G 蛋白的通路也会在 PTH1R 下游被激活。骨细胞：骨重塑的推动者微损伤或激素/化学刺激改变引起的骨细胞凋亡可能通过向周围骨细胞发送信号来启动针对性的骨重塑，这些周围骨细胞随后会改变促/抑制破骨细胞生成的细胞因子（RANKL、M-CSF、OPG）的表达，从而招募破骨细胞（和/或前体细胞）。骨细胞还会表达一些调节骨形成的因子，比如SOST-骨硬化素和Dkk1，这会影响成骨细胞的生成和功能。糖尿病、骨细胞和PTH1R通路糖尿病会导致骨细胞凋亡增加、骨形成减少、骨吸收增加，同时骨髓脂肪组织积累增加，这些因素综合起来会引起骨丢失、骨皮质和骨小梁变薄、骨皮质多孔以及骨脆性。直接激活骨细胞中的PTH1R可以通过激活激酶通路、调节骨细胞衍生因子的表达，并与机械刺激协同作用，从而纠正糖尿病对骨骼的破坏作用。糖尿病中骨骼对增肌疗法的反应激活PTH1R/SOST-骨桥蛋白轴可以逆转糖尿病骨特征。PTH1R配体和通过Scl-Ab直接抑制SOST-骨桥蛋白都能增加骨形成、骨量和骨强度。此外，与PTH和ABL相比，Scl-Ab通过抑制骨吸收带来更高的骨量增加，并恢复皮质骨厚度和力学性能。糖尿病引起的骨病疗法：抗吸收药物vs.促合成药物糖尿病引起的骨质脆弱的标准治疗是抗骨吸收疗法，这类疗法能有效阻止骨吸收及相关的骨质流失。然而，抑制骨吸收并不能增加骨形成，因此无法重建骨骼或修复糖尿病骨骼所表现出的损伤微结构。相比之下，三种获FDA批准、具骨生成特性的疗法——特立帕肽、阿巴帕肽和罗莫索单抗——能够纠正糖尿病对骨量、组织结构和强度的影响，恢复成骨细胞数量和活性，并使骨转录组特征恢复正常。这些前临床研究成果为在糖尿病中使用骨生成疗法恢复骨强度，以及更新标准治疗奠定了基础。总结与评论： PTH1R作为调节钙稳态和骨代谢的核心受体，其功能异常直接关联多种骨代谢疾病和肾脏疾病。靶向PTH1R的药物从早期的特立帕肽发展到阿巴帕肽等新型药物，治疗效果显著。未来研究方向包括开发更加便捷的给药系统、探索信号通路选择性激活的药物以及拓展在肾脏疾病、肝纤维化等领域的应用潜力。靶向PTH1R的精准治疗策略有望在更广泛的疾病领域发挥重要作用。

2026-10-19

·任卫东医生团队科普

骨质疏松治疗——地舒单抗使用要点速览！

温馨提示：由于微信修改了推送规则，需读者经常点“在看”“点赞”，否则会逐渐收不到推文！请将“任卫东医生团队科普”设为星标或每次看完后点击一下页面下端的“在看”“点赞”，谢谢！骨质疏松及骨质疏松性骨折已成为全球重大公共卫生挑战。随着临床医学的发展，骨质疏松的干预策略正经历从传统化学类药物向靶向生物制剂的深刻变革。《地舒单抗治疗骨质疏松临床应用指南（2026）》（以下简称"指南"）基于循证医学证据，围绕地舒单抗适应证与禁忌证、用法用量及治疗方案、停药指征与序贯治疗策略、联合用药原则、安全性评价及罕见不良反应监测、特殊人群用药（包括肾功能不全、骨质疏松性骨折、男性骨质疏松及糖尿病伴骨折风险患者等）等关键临床问题提出27条核心推荐意见，为临床规范化应用提供指导。表1 地舒单抗中国获批产品一、规范用药：适应人群与初始治疗策略指南明确了地舒单抗的适用人群、绝对禁忌症及合并不同并发症患者的用药原则，确认其在绝经后女性、男性和糖皮质激素性骨质疏松中的广泛适用性，并为肾功能不全及糖尿病患者的安全用药提供了循证依据。 1.适应证：骨折高风险的绝经后妇女的骨质疏松症、骨折高风险的男性骨质疏松症、骨折高风险的糖皮质激素性骨质疏松症。 2.禁忌证：低钙血症。 3.用法用量：地舒单抗，60 mg，皮下注射，每 6 个月 1 次。 4.对于不能使用口服药物治疗的骨折高风险患者可考虑使用阿巴帕肽、地舒单抗、罗莫索珠单抗、特立帕肽和唑来膦酸作为初始治疗（推荐等级：A 级，证据等级：1）。 5.可用于糖皮质激素诱导性骨质疏松症（GIOP）等继发性骨质疏松症患者。 6.肾功能不全的骨质疏松症患者，可酌情考虑使用地舒单抗和维生素 K2，但应注意摄入足够的钙和维生素 D。 7.推荐地舒单抗作为男性骨质疏松症抗骨质疏松药物。 8.地舒单抗可用于治疗有骨折风险的糖尿病患者。二、长期主义：疗效评估与“无药物假期”用药原则地舒单抗不经肝脏代谢且不沉积于骨基质。长达10年的数据证实其具有持续增加骨密度的能力，因此指南确立了须制定长期计划且“不存在药物假期”的核心原则。 9.开始使用地舒单抗之前，应制定长期的个性化 OP 管理计划，并让患者和初级保健从业者都意识到在未与医疗专业人员商讨的情况下，不应停止或延迟地舒单抗的治疗（强烈推荐）。 10.对于正在使用地舒单抗治疗的绝经后女性，推荐其在 5～10 年后重新评估骨折风险。对于那些仍然存在骨折高风险的女性应该继续使用地舒单抗或其他抗 OP 疗法治疗（推荐等级：2级）。 11.地舒单抗安全性较好，但使用时应注意其作用时间短，不存在药物假期。关于药物假期，仅适用于双膦酸盐药物，除双膦酸盐外，其他抗骨质疏松症药物均无药物假期，地舒单抗治疗 5 ～ 10 年后应重新评估骨折风险。地舒单抗长期治疗可持续提升各部位 BMD，无平台期，不会在骨基质中沉积，无需“药物假期”。地舒单抗持续使用 10 年，BMD 仍维持增长，且安全性良好，如果停用，应立刻使用其他骨吸收抑制剂。已有连续使用 10 年的临床报告。三、严控停药反弹：规范化序贯转换与替代方案指南指出，严控停药后的骨折风险反弹是临床管控的重中之重。停用地舒单抗会导致破骨细胞活性迅速反弹，极易引发快速骨丢失及多发性椎体骨折。 12.避免非计划停止使用地舒单抗，因为停药会导致椎体骨折风险增加，因此在不考虑替代治疗的情况下不得停止使用（强烈推荐）。 13.如果要停用地舒单抗，建议在使用最后一次地舒单抗的 6 个月后静脉注射唑来膦酸，随后监测血清 CTX，以指导进一步治疗的时间（强烈推荐）。在无法监测血清 CTX 的情况下，建议在注射第一剂唑来膦酸 6 个月后再次注射唑来膦酸（条件推荐）。 14.多部国内外指南推荐优先选用已被证实可降低椎体骨折、非椎体骨折和髋部骨折风险的药物进行治疗，并应定期监测其耐受性和患者的依从性。对于口服不耐受双膦酸盐、患有痴呆、吸收不良和依从性不佳的患者，建议静脉注射唑来膦酸或皮下注射地舒单抗进行治疗（推荐等级：A 级，证据等级：IB 级）。 15.停用地舒单抗治疗后，若无禁忌证，建议使用另外一种抗骨吸收药物进行治疗（推荐等级：A 级，证据等级： 1）。 16.对于正在使用地舒单抗治疗的绝经后女性，在其无后续抗重吸收或其他预防骨转换反弹、减少 BMD 快速下降及骨折风险增加的措施时，不得停止使用地舒单抗（未分级，但有充足的临床证据）。 17.地舒单抗停药的建议：临床医师应建议长期接受≥24 个月（4次剂量）治疗的患者避免擅自停止地舒单抗。地舒单抗停药后转用双膦酸盐的患者，应每年进行一次 DXA 骨密度检测，或在有实验室检测条件的情况下，缩短检测间隔至 3 ～ 6 个月，以监测 BTMS 的变化。 18.关于地舒单抗序贯治疗的建议：如果需要药物转换，原则上只要遵循新药的禁忌证，可以直接转换到新药，从相对强度较低的骨吸收抑制剂（如雷洛昔芬或 HRT）转换到更强效的骨吸收抑制剂（如双膦酸盐或地舒单抗），无需额外特殊处理，无需时间间隔。该原则同样适用于从口服/静脉注射双膦酸盐转换到地舒单抗。可以直接从口服双膦酸盐转换至地舒单抗，也可以在唑来膦酸计划的下一剂给药日，直接转换至地舒单抗，必要时可以提前转换，且无禁忌。从口服双膦酸盐转换至地舒单抗预计会使所有部位的 BMD 均能获得更好改善。从地舒单抗转换至口服 /静脉注射双膦酸盐时，患者必须充分了解快速骨丢失和多发性椎体骨折的潜在风险。 19.地舒单抗联合特立帕肽治疗能更好增加骨密度，酌情用于骨折极高风险的患者。序贯治疗方案：特立帕肽序贯双膦酸盐或地舒单抗治疗，是较为合适的序贯治疗模式。四、特殊人群用药：骨折与围术期靶向干预骨折及围手术期是骨量快速流失的危险窗口。指南对髋膝关节置换、肩关节周围骨折等特定时期的用药给予建议。 20.建议拟行髋膝关节置换术合并骨质疏松的患者，围手术期及术后，在充足补充钙剂、活性维生素 D 等基础治疗的前提下，结合患者的骨质疏松严重程度和个体化需求，选择适宜的药物（如双膦酸盐、地舒单抗、甲状旁腺素类似物、罗莫索珠单抗等）进行干预。 21.推荐在骨质疏松性肩关节周围骨折手术围术期抗骨质疏松治疗应包括基础补充和骨代谢药物两部分，其中基础补充部分应同时覆盖钙剂和维生素 D 制剂（推荐强度：强）。围术期卧床患者发生快速骨丢失，应酌情使用骨吸收抑制类药物，如双膦酸盐或地舒单抗等，有助于维持内固定稳定。 22.老年髋部脆性骨折患者应优先选用具有较广抗骨折谱的抗骨质疏松药物；建议使用注射制剂如地舒单抗。 23.脆性骨折术后抗骨质疏松治疗可以优先考虑抗骨吸收药物。地舒单抗因其良好的安全性和有效性可作为一种选择（推荐等级：1A 级）。五、筑牢安全防线：不良反应监测与用药协同鉴于地舒单抗具有强效抑制骨吸收的作用，低钙血症是其最常见的不良反应。指南围绕其不良反应提出了明确的监测与管理建议，包括血钙水平监测、钙剂与维生素D的常规补充，以及颌骨坏死等罕见不良反应的识别与防控。 24.使用地舒单抗前，推荐评估患者血钙水平，纠正低钙血症; 接受这类药物治疗的患者，推荐同时补充足量的钙剂和维生素D，且治疗期间监测血钙水平（证据级别：5，推荐等级：D）。适时检测骨代谢指标。 25.地舒单抗主要不良反应是低钙血症，特别是存在维生素 D 缺乏症及肾脏损害的情况下。对易患低钙血症者，建议每次使用地舒单抗前及第一次使用后 2 周监测血清钙水平。另外，地舒单抗可能引起严重感染，包括膀胱炎、上呼吸道感染、肺炎、皮肤蜂窝组织炎等，可能与 RANKL 在免疫系统中的作用有关。长期应用地舒单抗可能会过度抑制骨吸收，出现下颌骨坏死或非典型性股骨骨折。其他不良反应包括皮疹、皮肤瘙痒、肌肉或骨痛等。存在高度骨折风险患者，特别是已存在椎体骨折的患者，停用地舒单抗可能会增加多发性椎体骨折的风险。因此，如果考虑停止治疗，应改用其他抗骨吸收药物维持。常规联合应用维生素 D 和钙。 26.罕见不良反应：地舒单抗相关颌骨坏死的报道相对于双酸盐类药物数量较少。在Freedom的 10 年研究中累计有 13 例颌骨坏死病例，校正后每年每 10 000 受试者中有 5. 2 例发病，且经过恰当的处理可全部治愈。回顾性和前瞻性数据均显示超过 90%的颌骨坏死病例发生在接受高剂量地舒单抗治疗的肿瘤患者中，并且发病率随用药时间延长而增加。 27.推荐 OP 社区干预的药物包括骨吸收抑制剂（双膦酸盐类、降钙素类、地舒单抗、SERM、雌激素）、骨形成促进剂（甲状旁腺素类似物）、其他机制类药物、中药等，需在二级或三级医院专科医生指导下进行个体化治疗。来源：《地舒单抗治疗骨质疏松临床应用指南（2026）》编写组.地舒单抗治疗骨质疏松临床应用指南（2026）中国骨质疏松杂志, 2026 河北北方学院附属第一医院内分泌科简介 1989年成立内分泌专业组，2003年独立门诊，2006年独立病房，2011年独立病区。内分泌科是张家口市内分泌代谢专业唯一具有硕士研究生招收与培养资质的科室，张家口市唯一具有内科学（内分泌代谢）专业国家级住院医师规范化培训招收与培养资质的科室。国家级药物临床试验质量规范（GCP）备案专业，中华医学会糖尿病健康教育管理认证单位，糖尿病院内血糖管理培训实践基地，河北省生长发育与矮小症专病联盟单位，河北省罕见病成员单位，共青团河北省青年文明号。多次承办河北省省级继续教育项目和国家级继续教育项目，曾多次获得过院级的“先进科室”、“先进护理集体”等称号。内分泌科将努力建成医德高尚、医术精湛、服务优质、团结协作的学习型团队，集医教研于一体、以内分泌代谢疾病为诊疗特色的京西北区域国家重点内分泌专科。内分泌科年门诊量6.4万人次，病房床位68张，年住院2021人次。内分泌科现有医生17人，其中主任医师2人，副主任医师5人，主治医师6人，住院医师4人。内分泌科现有护士17人，其中主管护师7人，有2名护士持有糖尿病教育专科护士证。内分泌学科是院级重点学科，开设有内分泌专家门诊、生长发育门诊、肾上腺门诊、肥胖门诊、甲状腺门诊、普通门诊、宣教门诊。糖尿病与甲状腺疾病为内分泌科常见疾病，目前内分泌科开展的亚专业包括生长发育、内分泌高血压、肥胖和特殊类型糖尿病，涉及病种包括糖尿病、甲状腺疾病、生长发育异常、肾上腺疾病、垂体疾病、性腺疾病、骨质疏松、肥胖等内分泌代谢疾病。内分泌科联系电话：0313-80415138041512一附院内分泌科团队与好大夫在线联合推出内分泌代谢疾病网上诊室服务！请您通过手机下载“好大夫在线”APP，登录或者注册后申请线上问诊就可以。以下是内分泌科医生的网上诊室二维码，如果您已经登记网上诊室，请您直接申请网上问诊，不要重复扫码报到。河北北方学院附属第一医院内分泌科团队竭诚为您提供优质的医疗护理服务！如果您觉得本文内容对他人有所帮助可以转发到朋友圈或转给有需要的人长按二维码，即可关注本微信公众号内分泌科医办室：0313-8041513 无恒难以做医生，做任何学问都要勤奋和持久，学医尤需如此。医生这个职业的特殊之处在于，一举手一投足都接触病人，医术好些精些，随时可以活人，医术差些粗些，随时可以害人。一个医生，如果不刻苦学习，医术上甘于粗疏，就是对病人的生命不负责任。当然，就是勤奋学习，也不等于就能万全地解决疾病。但无怠于学，至少可以无愧于心。声明：凡注明来源的均属转载，转载只限于分享专业知识和医学信息之用,不用于任何商业用途。文章版权归原作者所有。如果所选内容的文章作者认为其作品不宜供大家浏览或者不应无偿使用，如果侵犯了您的权益，请及时联系我们邮箱:rwdlln@126.com，我们会及时改正或删除，谢谢

2026-10-19

·BioSpace

Paratek Pharmaceuticals to Present New Data on NUZYRA® (omadacycline) at IDWeek 2026

Highlights include clinical and non-clinical data from Company- and investigator-sponsored studies KING OF PRUSSIA, Pa., Oct. 19, 2026 (GLOBE NEWSWIRE) -- Paratek Pharmaceuticals, Inc., a privately held specialty pharmaceutical company focused on high-need therapeutic areas, today announced that new data from scientific and investigator-initiated studies of NUZYRA ® (omadacycline) will be presented at IDWeek 2026 in Washington, D.C., October 21-24. “Paratek is proud to continue advancing the science of infectious disease and expanding the body of research around omadacycline,” said Randy Brenner, Chief Development and Regulatory Officer at Paratek. “The data being presented at IDWeek reflect the breadth of scientific inquiry underway across a range of pathogens and infectious disease settings. We are pleased to support continued scientific inquiry and dialogue around these important areas of need.” IDWeek 2026 Poster Sessions Poster Title: In Vitro Activity of Omadacycline against 7,200 Bacterial Clinical Isolates Representing Multiple Infection Types from the United States (2024–2025) Session: C3. Skin and soft tissue Presenter: Michael D. Huband, BS (Paratek research) Session Date, Time: Saturday, Oct. 24, 12:15 p.m. – 1:30 p.m. ET Location: Poster Hall B-C Poster ID: P-383 (The study has been supported in whole or part with federal funds from the Department of Health and Human Services; Administration for Strategic Preparedness and Response; Biomedical Advanced Research and Development Authority (BARDA) under contract number 75A50120C00001.) Poster Title: Activity of Omadacycline and Comparators Against Common Microbial Contaminants: Cronobacter sakazakii , Pluralibacter gergoviae , and Burkholderia cepacia species complex Isolates Session: C6. Enteric infection Presenter: Michael D. Huband, BS (Paratek research) Session Date, Time: Saturday, Oct. 24, 12:15 p.m. – 1:30 p.m. ET Location: Poster Hall B-C Poster ID: P-488 Poster Title: In Vitro Activity of Omadacycline Against Borrelia spp. and Bartonella henselae Session: A4. Treatment of antimicrobial-resistant infections Presenter: J.V. Pierce, PhD (Paratek research) Session Date, Time: Thursday, Oct. 22, 12:15 p.m. – 1:30 p.m. ET Location: Poster Hall B-C Poster ID: P-122 Poster Title: Mycobacterium avium Complex Pulmonary Infections Treated with Regimens Containing Omadacycline in a Veteran Population Session: K. Tuberculosis and other Mycobacterial Infections Presenter: Olivia G. Funk, PharmD (Investigator-initiated research) Session Date, Time: Friday, Oct. 23, 12:15 p.m. – 1:30 p.m. ET Location: Poster Hall B-C Poster ID: P-1345 About Paratek Pharmaceuticals, Inc. Paratek Pharmaceuticals, Inc. is a specialty pharmaceutical company with a portfolio of differentiated medicines serving patients across multiple therapeutic areas. The company integrates and advances commercial-stage assets through disciplined commercial execution, lifecycle management, and clinical development initiatives designed to expand and strengthen its portfolio. Paratek's products include NUZYRA ® (omadacycline), XHANCE ® (fluticasone propionate), and TYMLOS ® (abaloparatide). Paratek is privately held by B-FLEXION Life Sciences. In December 2019, BARDA awarded Paratek a PBS contract (75A50120C00001) that is now valued at up to approximately $304 million. In addition to supporting the development of NUZYRA for both the treatment and prophylaxis of pulmonary anthrax, this contract supports the U.S. onshoring of NUZYRA and manufacturing security requirements; FDA post-marketing requirements associated with the initial NUZYRA approval; and the procurement of up to 10,000 treatment courses of NUZYRA for the treatment of anthrax. For more information, visit or follow us on LinkedIn and X . About NUZYRA NUZYRA (omadacycline) is an antibiotic with both once-daily oral and intravenous (IV) formulations indicated for the treatment of community-acquired bacterial pneumonia (CABP) and acute bacterial skin and skin structure infections (ABSSSI) caused by susceptible microorganisms. A next-generation tetracycline, NUZYRA is specifically designed to overcome tetracycline resistance and exhibits activity across a spectrum of bacteria, including Gram-positive, Gram-negative, atypical, and other drug-resistant strains. IMPORTANT SAFETY INFORMATION CONTRAINDICATIONS NUZYRA is contraindicated in patients with known hypersensitivity to omadacycline or tetracycline class antibacterial drugs, or to any of the excipients. WARNINGS AND PRECAUTIONS Permanent tooth discoloration and enamel hypoplasia may occur with the use of NUZYRA during tooth development (last half of pregnancy, infancy, and childhood to the age of 8 years). Reversible inhibition of bone growth may occur with the use of NUZYRA during the second and third trimester of pregnancy, infancy, and childhood up to the age of 8 years. Hypersensitivity reactions have been reported with NUZYRA. Life-threatening hypersensitivity (anaphylactic) reactions have been reported with other tetracycline class antibacterial drugs. NUZYRA is structurally similar to other tetracycline class antibacterial drugs and is contraindicated in patients with known hypersensitivity to tetracycline class antibacterial drugs. Discontinue NUZYRA if an allergic reaction occurs. Clostridioides difficile -associated diarrhea (CDAD) has been reported with use of nearly all antibacterial agents and may range in severity from mild diarrhea to fatal colitis. Evaluate if diarrhea occurs. Tetracycline class effects may occur with NUZYRA. Adverse reactions, including photosensitivity, fixed drug eruption, pseudotumor cerebri, and anti-anabolic action (which has led to increased BUN, azotemia, acidosis, hyperphosphatemia, pancreatitis, and abnormal liver function tests), have been reported for other tetracycline class antibacterial drugs, and may occur with NUZYRA. Discontinue NUZYRA if any of these adverse reactions are suspected. Risk of the development of drug-resistant bacteria is increased when prescribing NUZYRA in the absence of a proven or strongly suspected bacterial infection or a prophylactic indication and is unlikely to provide benefit to the patient. ADVERSE REACTIONS CABP: The most common adverse reactions (incidence ≥2%) are alanine aminotransferase increased, headache, hypertension, and aspartate aminotransferase increased. ABSSSI: The most common adverse reactions (incidence ≥2%) are nausea, vomiting, infusion site reactions, alanine aminotransferase increased, aspartate aminotransferase increased, headache, and diarrhea. DRUG INTERACTIONS Patients who are on anticoagulant therapy may require downward adjustment of their anticoagulant dosage while taking NUZYRA. Absorption of tetracyclines, including NUZYRA, is impaired by antacids containing aluminum, calcium, or magnesium, bismuth subsalicylate, and iron containing preparations. USE IN SPECIFIC POPULATIONS Lactation: Breastfeeding is not recommended during treatment with NUZYRA. See full prescribing information here . MEDIA CONTACT: media@paratek.com

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100 项与阿巴帕肽相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10885	阿巴帕肽	H05AA H05AA04	DB05084

研发状态

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10 条最早获批的记录,

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适应症	国家/地区	公司	日期
骨质疏松症	日本	Teijin Ltd.	2022-08-31
绝经期后骨质疏松	美国	Radius Health, Inc.	2017-04-28

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适应症	最高研发状态	国家/地区	公司	日期
原发性骨质疏松症	临床3期	美国	Radius Health, Inc.	2018-05-03
原发性骨质疏松症	临床3期	意大利	Radius Health, Inc.	2018-05-03
原发性骨质疏松症	临床3期	波兰	Radius Health, Inc.	2018-05-03
骨折	临床3期	美国	Radius Health, Inc.	2011-04-01
骨折	临床3期	阿根廷	Radius Health, Inc.	2011-04-01
骨折	临床3期	巴西	Radius Health, Inc.	2011-04-01
骨折	临床3期	捷克	Radius Health, Inc.	2011-04-01
骨折	临床3期	丹麦	Radius Health, Inc.	2011-04-01
骨折	临床3期	爱沙尼亚	Radius Health, Inc.	2011-04-01
骨折	临床3期	中国香港	Radius Health, Inc.	2011-04-01

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04167163 (Pubmed \| JB JS Open Access)	临床4期	骨质疏松症	58	Abaloparatide	遞獵觸糧繭構糧獵遞製(顧網網壓餘齋鹽衊製餘) = 願鏇醖齋鏇淵選淵範獵積願齋製壓構膚鑰齋願 (願鹽壓觸蓋範築膚繭構 ) 更多	积极	2026-07-01
ENDO2026	N/A	髋部骨折	5,914	Abaloparatide + Abaloparatideantiresorptive therapy	繭製蓋窪網膚鬱網積鏇(窪鑰構鹽壓觸顧遞築襯) = 鹹壓選蓋廠窪鏇餘膚鏇齋選膚醖齋襯鹹簾遞獵 (餘壓構糧鹽範鑰鬱醖膚 )	积极	2026-06-14
				Teriparatide	繭製蓋窪網膚鬱網積鏇(襯窪鬱築艱餘糧夢壓簾) = 遞壓鏇夢鹹膚觸鏇遞鹹壓遞鏇簾鹽鏇蓋顧鏇獵 (遞窪鹹築積鹹鑰鑰觸顧 )
WCO_IOF_ESCEO2026	N/A	骨质疏松症	43	Abaloparatide	範選鑰鹽顧餘壓膚憲選(獵製鏇艱觸衊願獵鏇餘) = 遞壓製鏇築鏇窪遞範積餘淵構觸衊夢觸構鬱蓋 (鏇壓顧蓋積製遞艱觸製 ) 更多	积极	2026-04-16
WCO_IOF_ESCEO2026	N/A	-	168	Romosozumab	網齋艱壓鏇夢鑰鏇淵糧(壓繭簾艱夢糧衊遞簾淵) = 廠鹽衊築艱廠鹽蓋窪構鏇膚鹽夢繭網艱顧構鏇 (鹽鬱淵鏇獵築窪衊蓋築 )	积极	2026-04-16
				Teriparatide	網齋艱壓鏇夢鑰鏇淵糧(壓繭簾艱夢糧衊遞簾淵) = 顧壓艱廠糧製顧壓廠網鏇膚鹽夢繭網艱顧構鏇 (鹽鬱淵鏇獵築窪衊蓋築 )
WCO_IOF_ESCEO2026	N/A	骨质疏松性骨折	258	Denosumab	顧願觸積顧醖膚餘繭糧(窪觸醖顧構遞製夢膚築) = 簾鹹遞廠鬱願襯衊壓鹹遞糧廠壓窪窪艱膚鬱築 (遞醖醖襯積餘範膚廠網 ) 更多	积极	2026-04-16
ENDO2025	N/A	骨质疏松症	42,900	Abaloparatide [ABL]	獵鑰願糧顧範夢壓醖鬱(築齋淵膚廠製鹽築艱繭) = 餘膚餘鏇簾顧襯糧壓構鬱餘鏇築構餘積選築簾 (淵獵壓糧鑰網築獵齋製, 5.8) 更多	不佳	2025-07-12
				Teriparatide [TPTD]	獵鑰願糧顧範夢壓醖鬱(築齋淵膚廠製鹽築艱繭) = 顧醖選鑰願積糧願齋製鬱餘鏇築構餘積選築簾 (淵獵壓糧鑰網築獵齋製, 5.6) 更多
NCT01343004 (ACTIVE, Pubmed \| Menopause)	临床3期	骨质疏松性骨折	-	Abaloparatide	壓願餘醖襯網餘築構網(廠遞選築糧窪壓簾壓範) = 8.9% 衊積醖製淵齋構製鏇憲 (襯壓壓襯膚構簾夢顧選 ) 更多	积极	2025-05-01
				Placebo
WCO_IOF_ESCEO2025	N/A	骨质疏松症	69	Abaloparatide	構構淵鹽憲膚齋願齋簾(遞網範築範繭範壓夢憲) = 鏇淵鏇膚鹹獵觸夢衊襯蓋衊鏇選觸獵構廠觸襯 (範鑰鬱廠鬱膚遞鏇憲簾 ) 更多	积极	2025-04-10
NCT04760782 (CTgov)	临床2期	骨折	22	Hard collar immobilization+Abaloparatide (Treatment Group)	夢鑰鏇網齋鏇製醖憲簾(糧廠淵顧鬱淵觸蓋壓顧) = 鏇膚製繭鑰積餘醖醖積餘願選夢鬱網窪範獵製 (選簾願鬱繭夢鹽顧製鑰, 範壓窪鑰膚鹹構構觸鏇 ~ 製獵觸積積齋繭餘簾衊) 更多	-	2024-09-19
				Hard collar immobilization (Historical Control Group)	夢鑰鏇網齋鏇製醖憲簾(糧廠淵顧鬱淵觸蓋壓顧) = 蓋繭衊壓夢蓋糧淵網製餘願選夢鬱網窪範獵製 (選簾願鬱繭夢鹽顧製鑰, 鏇醖夢膚顧膚襯鑰網顧 ~ 鏇築遞觸憲壓衊鏇選襯) 更多
NCT03512262 (ATOM, ENDO2024)	临床3期	骨硬化 PINP \| CTX	228	Abaloparatide 80 µg	繭夢憲壓鹽蓋遞願觸餘(構壓鑰襯夢顧淵顧糧醖) = 築憲積選鬱遞範鏇廠鹽積鏇齋鹽蓋膚襯構遞餘 (齋鬱壓膚觸築顧鏇膚繭 ) 更多	积极	2024-06-01