BGM-0504

SUZHOU, China 中国苏州, ，May 12, 2026 2026年5月12日/PRNewswire/ -- As competition in the weight loss drug market progressively intensifies, the latest Phase III clinical data disclosed by BrightGene Bio-Medical (688166.SH) for BGM0504 has reignited market attention. /PRNewswire/ -- 随着减肥药市场竞争日益激烈，博瑞生物医药（688166.SH）最新披露的BGM0504三期临床数据再次引起了市场关注。Mean weight reduction of 19.3%, waist circumference decrease of 16.5 cm, systolic blood pressure reduction of 22.9 mmHg in the hypertensive population, alongside uric acid reduction of 70.7 μmol/L, triglyceride reduction of 33.6%, bone mineral density showing improvement rather than decline despite weight loss, and a discontinuation rate of 0.7% in the high-dose group. 平均体重减轻19.3%，腰围减少16.5厘米，高血压人群收缩压降低22.9 mmHg，尿酸降低70.7 μmol/L，甘油三酯减少33.6%，骨密度在减重的同时有所改善而非下降，高剂量组的停药率为0.7%。If these metrics appeared individually, their significance would primarily reflect efficacy enhancement; however, when multiple parameters are simultaneously achieved in a single product, such therapies extend from singular weight management toward comprehensive metabolic management.. 如果这些指标单独出现，它们的意义主要在于反映疗效的提升；然而，当多个参数在单一产品中同时实现时，此类疗法便从单一的体重管理扩展到全面的代谢管理。Against this backdrop, a target previously regarded largely as a supporting player is now entering the core spotlight: GIP. 在这种背景下，一个之前被视为主要配角的目标现在正进入核心焦点：GIP。Over the past decade-plus, 在过去的十多年里，GLP-1 GLP-1has defined the business model for weight loss drugs—high-value innovative therapeutics driven by weight reduction as the core endpoint. As the dual-agonist era advances, the role of GIP is undergoing transformation, evolving from its early perception as primarily contributing to tolerability modulation toward becoming a critical variable in metabolic architecture regulation. 已经为减肥药物定义了商业模式——以减重为核心终点的高价值创新疗法。随着双激动剂时代的推进，GIP 的作用正在发生转变，从早期被认为主要参与耐受性调节，逐渐演变为代谢结构调控中的关键变量。The significance of this shift lies not merely in adding another target, but in the broader metabolic effects associated with GIP activation.. 这种转变的意义不仅仅在于增加另一个靶点，而在于与GIP激活相关的更广泛的代谢效应。From a Single Endpoint to Multi-Parameter Synergy 从单一终端到多参数协同From an innovation trajectory standpoint, the weight-management space has already undergone a clear upgrade cycle. 从创新轨迹的角度来看，体重管理领域已经经历了一个明显的升级周期。Single-target 单目标GLP-1 GLP-1drugs, with its core value primarily reflected in weight loss and glycemic control, while effects on blood pressure, lipids, and other parameters have largely been secondary, accompanying improvements. Subsequently, dual agonists pushed weight loss magnitude closer to the ~20% range and extended benefits across certain metabolic markers, but overall market pricing has still been anchored to weight reduction and glucose lowering as the primary endpoints.. 药物，其核心价值主要体现在减重和血糖控制上，而对血压、血脂等其他参数的影响大多为次要的伴随改善。随后，双重激动剂将减重幅度提升至约 20% 的范围，并扩展了某些代谢指标的益处，但整体市场定价仍以减重和降糖作为主要终点。Against this backdrop, BGM0504's distinguishing feature is not a breakthrough in any single metric, but rather the coordinated improvement across multiple endpoints. 在此背景下，BGM0504 的显著特点并不是单一指标的突破，而是多个终点指标的协同改善。A 16.5 cm reduction in waist circumference suggests a direct impact on visceral fat—a core risk driver—rather than an effect limited to body weight alone. A blood pressure reduction of more than 20 mmHg, together with a target achievement rate above 90%, moves the effect from 'ancillary improvement' into a clinically actionable range. 腰围减少16.5厘米，这表明对内脏脂肪——一个核心风险驱动因素——产生了直接影响，而不仅仅是局限于体重的变化。血压降低超过20毫米汞柱，再加上高于90%的目标达成率，使得这种效果从“辅助性改善”进入了临床可操作范围。A 70.7 μmol/L decrease in uric acid and a triglyceride reduction of more than 30% are approaching the magnitude typically seen with dedicated metabolic therapies.. 尿酸减少70.7 μmol/L，甘油三酯降低超过30%，这一幅度接近通常在专门的代谢疗法中所见的水平。More importantly, in the context of nearly 20% weight loss, bone mineral density did not decline but instead increased, while the discontinuation rate remained at a low 0.7%. This indicates that improved efficacy was not achieved at the expense of bone loss or reduced treatment adherence. 更重要的是，在接近 20% 的体重减轻的情况下，骨密度没有下降反而增加，同时停药率仍然保持在 0.7% 的低水平。这表明疗效的提升并非以骨质流失或治疗依从性降低为代价。When a single drug can simultaneously improve body weight, blood pressure, blood lipids and uric acid, it demonstrates effects across multiple chronic disease populations. 当一种药物能够同时改善体重、血压、血脂和尿酸时，它就展示了对多种慢性疾病人群的疗效。From Mechanism to Differentiation: The Emerging Role of GIP 从机制到分化：GIP的新兴作用If the Phase III clinical data of BGM0504 represent the outcomes, the mechanism determines whether these outcomes are explainable and sustainable. 如果BGM0504的III期临床数据代表结果，那么机制决定了这些结果是否可解释且可持续。Within the GLP–1 pathway, weight loss primarily stems from intake control, achieved via appetite suppression and delayed gastric emptying. Improvements in blood pressure, lipid profile, and other markers are largely secondary consequences of weight reduction. 在GLP-1 通路中，体重减轻主要源于通过抑制食欲和延缓胃排空实现的摄入控制。血压、血脂和其他标志物的改善在很大程度上是体重减轻的次要结果。In contrast, GIP acts more as an intrinsic regulatory variable within the metabolic system. The GIP receptor is highly expressed in adipose tissue. Upon activation, it modulates adipose tissue blood flow and inflammatory status, thereby regulating fat distribution. This process not only affects body fat percentage but also drives coordinated improvements across multiple parameters—including blood lipids and blood pressure—by enhancing insulin sensitivity.. 相比之下，GIP更多地作为代谢系统内的内在调节变量。GIP受体在脂肪组织中高度表达，激活后可调节脂肪组织的血流量和炎症状态，从而调控脂肪分布。这一过程不仅影响体脂百分比，还通过增强胰岛素敏感性，推动血脂、血压等多项指标的协同改善。From the Phase III data of BGM0504, a clear correlation can be observed with this mechanistic pathway. A 16.5 cm reduction in waist circumference indicates an impact on visceral fat, a key cardiometabolic risk factor. A 33.6% decrease in triglycerides, along with reduced LDL–C and elevated HDL–C, demonstrates favorable remodeling of lipid metabolism. 从BGM0504的III期数据中，可以明显观察到与该机制途径的相关性。腰围减少16.5厘米表明对内脏脂肪产生了影响，而内脏脂肪是关键的心脏代谢风险因素。甘油三酯降低33.6%，同时低密度脂蛋白胆固醇（LDL-C）减少和高密度脂蛋白胆固醇（HDL-C）升高，显示出脂质代谢的有利重塑。A 70.7 μmol/L reduction in uric acid can be regarded as a coordinated outcome of an optimized metabolic milieu.. 尿酸降低70.7 μmol/L可视为优化代谢环境的协调结果。For blood pressure, multiple factors act in concert—including reduced adipose inflammation, improved insulin resistance, and enhanced vascular endothelial function—leading to a systolic blood pressure reduction of over 22.9 mmHg and a 92.9% control rate in patients with concomitant hypertension. This profile reflects a holistic, metabolism–driven regulatory effect.. 对于血压，多种因素协同作用——包括减少脂肪炎症、改善胰岛素抵抗和增强血管内皮功能——使合并高血压患者的收缩压降低超过22.9 mmHg，控制率达到92.9%。这一特征反映了整体的、代谢驱动的调节效应。At the lipid metabolism level, GIP improves insulin sensitivity and modulates lipoprotein metabolism, thereby affecting hepatic synthesis and secretion of very-low-density lipoprotein (VLDL) while promoting triglyceride clearance in peripheral tissues. This results in a 33.6% reduction in triglycerides and optimized lipoprotein composition. 在脂质代谢水平上，GIP 提高胰岛素敏感性并调节脂蛋白代谢，从而影响肝脏极低密度脂蛋白（VLDL）的合成与分泌，同时促进外周组织中的甘油三酯清除。这导致甘油三酯水平降低 33.6%，并优化了脂蛋白组成。Changes in uric acid metabolism largely reflect a metabolic cascade effect. In obesity and insulin resistance, renal uric acid excretion is impaired. By improving insulin sensitivity, reducing adipose inflammation, and optimizing energy metabolism, GIP helps restore uric acid excretion balance.. 尿酸代谢的变化很大程度上反映了代谢级联效应。在肥胖和胰岛素抵抗中，肾脏尿酸排泄受到损害。通过改善胰岛素敏感性、减少脂肪炎症和优化能量代谢，GIP有助于恢复尿酸排泄平衡。Bone metabolism represents a distinctive feature of the GIP mechanism, supported by established human and mechanistic evidence. For instance, a study published in the 骨代谢是GIP机制的一个显著特征，得到了已确立的人体和机理证据的支持。例如，一项发表在Journal of Clinical Endocrinology & Metabolism 临床内分泌学与代谢杂志demonstrated that GIP significantly inhibits bone resorption independently of insulin. GIP receptors are expressed in osteoblasts; their activation promotes bone formation and suppresses bone resorption via regulation of the RANKL/OPG pathway, thereby contributing to bone remodeling. Moreover, GIP exerts additive effects when combined with . 证明了GIP独立于胰岛素显著抑制骨吸收。GIP受体在成骨细胞中表达；其激活通过调节RANKL/OPG通路促进骨形成并抑制骨吸收，从而促进骨骼重塑。此外，GIP与其它物质联合使用时发挥叠加效应。GLP-1 GLP-1. Multiple reviews have identified GIP as a key regulatory hormone in the gut–bone axis, mediating both bone resorption inhibition and bone formation modulation during postprandial bone remodeling. 多个评论已经将GIP确定为肠道-骨骼轴中的关键调节激素，在餐后骨骼重塑过程中介导骨吸收抑制和骨形成调节。Along the traditional single-target 沿着传统单一目标GLP-1 GLP-1pathway, rapid weight loss is often accompanied by declines in bone mineral density, and studies show that the addition of GIP offsets this risk. Accordingly, the absence of bone mineral density loss—and even an improving trend—despite substantial weight reduction can be mechanistically explained by a combination of reduced bone resorption, enhanced bone formation, and an optimized metabolic milieu. 途径，快速减重常常伴随着骨密度下降，研究表明添加GIP可以抵消这种风险。因此，尽管体重显著减少，但骨密度没有下降甚至出现改善趋势，这可以通过减少骨吸收、增强骨形成以及优化的代谢环境的综合作用来从机制上解释。This also provides mechanistic support for the long-term structural stability of dual-target therapies in chronic disease management.. 这还为慢性病管理中双靶点疗法的长期结构稳定性提供了机制支持。Overall, GIP is not merely an auxiliary target that amplifies weight loss. Rather, it participates in system-level regulation across multiple dimensions, including fat distribution, metabolic cross-talk, and maintenance of tissue homeostasis. When this pathway is effectively activated, a therapy's impact is no longer confined to the single endpoint of body weight, but extends across a broader set of metabolic parameters. 总体而言，GIP 并不仅仅是一个放大减重效果的辅助靶点。相反，它在脂肪分布、代谢交互以及组织稳态维持等多个维度上参与系统级调控。当这一通路被有效激活时，治疗的效果不再局限于体重这一单一终点，而是扩展到更广泛的代谢参数范围。This shift also offers a mechanistic basis for understanding BGM0504's concurrent improvements across multiple cardiometabolic indicators.. 这种转变也为理解BGM0504在多个心脏代谢指标上的同时改善提供了机制基础。BGM0504 is distinctive in that it deliberately increased the weighting of GIP at the design stage. According to a BGM0504 的显著特点是在设计阶段有意增加了 GIP 的权重。根据一个Nature - Scientific Reports 自然 - 科学报告publication, its dual-agonist activity is approximately three times that of tirzepatide. This difference is not merely a matter of 'stronger potency'; rather, at comparable dose levels, BGM0504 appears to achieve higher GIP receptor engagement and more efficient signaling activation, materially increasing GIP's contribution to the overall pharmacology.. 出版物中指出，其双激动剂活性约为替西帕肽的三倍。这种差异并不仅仅是“效力更强”的问题；相反，在相似剂量水平下，BGM0504似乎能够实现更高的GIP受体参与度和更高效的信号激活，实质性地增强了GIP对整体药理学的贡献。Within this architecture, 在此架构内，GLP-1 GLP-1and GIP take on differentiated roles: GIP 承担不同的角色：GLP-1 GLP-1provides the foundational effects on weight reduction and glycemic control, while GIP contributes more to fat distribution modulation, metabolic cross-talk, and tolerability optimization. 提供了减重和血糖控制的基础效应，而GIP则更多地贡献于脂肪分布调节、代谢交互作用及耐受性优化。From Product to Platform: GIP Is Poised to Drive a New Wave of Differentiation 从产品到平台：GIP 将推动新一轮差异化浪潮Once differentiation extends from mechanism into business model, shifts at the category level begin to emerge. Globally, the weight-management field is moving from single-target approaches toward multi-target combinations, along with expansion into multiple formulations and routes of administration. 一旦差异化从机制延伸到商业模式，类别的转变就开始显现。在全球范围内，体重管理领域正在从单一目标方法转向多目标组合，同时扩展到多种配方和给药途径。Beyond . 超出。GLP-1 GLP-1and GIP, oral options, amylin, muscle-preservation targets, and adipose signaling pathways are all becoming active frontiers of exploration. GIP、口服药物选项、艾米林、肌肉保护靶点以及脂肪信号通路都成为活跃的探索前沿。In this landscape, BrightGene Bio-Medical's strategy is closer to a platform-based approach. 在这种格局下，博瑞医药的战略更接近于平台化的思路。Building around BGM0504, the company has not only strengthened the GIP component of its mechanism, but has also advanced multiple parallel programs and modalities, including combinations of BGM0504 with amylin, an MSTN cyclic peptide, an ALK7-targeting siRNA, and several oral formulations. The goal is to assemble a systematic set of capabilities spanning adipose tissue, muscle, bone metabolism, and diverse dosing scenarios. 围绕BGM0504的开发，该公司不仅加强了其机制中的GIP成分，还推进了多个并行的项目和模式，包括将BGM0504与艾米林、一种MSTN环肽、一种靶向ALK7的siRNA以及多种口服制剂相结合。目标是构建一套系统的能力体系，涵盖脂肪组织、肌肉、骨骼代谢以及多样化的给药场景。In other words, the thesis is no longer simply to develop a single weight-loss drug, but to build a broader metabolic regulation platform.. 换句话说，这一理念不再仅仅是开发一种单一的减肥药物，而是构建一个更广泛的代谢调控平台。This brings us back to the original question: why was BGM0504 able to deliver consistent improvements across multiple endpoints at the same time? GIP affects multiple metabolic pathways. Clinical trials show that 这让我们回到最初的问题：为什么BGM0504能够同时在多个终点上带来持续的改善？GIP影响着多个代谢途径。临床试验显示，GLP-1 GLP-1/GIP dual agonists produce effects across body weight, glycemic control, blood pressure, lipid metabolism, and uric acid levels. GIP is increasingly emerging as a key variable shaping the next phase of differentiation in this space. /GIP双激动剂在体重、血糖控制、血压、脂质代谢和尿酸水平等方面产生作用。GIP正日益成为塑造这一领域下一阶段差异化的关键变量。SOURCE BrightGene 源代码 BrightGene21 21% %more press release views with 更多新闻发布视图与 Request a Demo 请求演示

SUZHOU, China , May 12, 2026 /PRNewswire/ -- As competition in the weight loss drug market progressively intensifies, the latest Phase III clinical data disclosed by BrightGene Bio-Medical (688166.SH) for BGM0504 has reignited market attention. Mean weight reduction of 19.3%, waist circumference decrease of 16.5 cm, systolic blood pressure reduction of 22.9 mmHg in the hypertensive population, alongside uric acid reduction of 70.7 μmol/L, triglyceride reduction of 33.6%, bone mineral density showing improvement rather than decline despite weight loss, and a discontinuation rate of 0.7% in the high-dose group. If these metrics appeared individually, their significance would primarily reflect efficacy enhancement; however, when multiple parameters are simultaneously achieved in a single product, such therapies extend from singular weight management toward comprehensive metabolic management. Against this backdrop, a target previously regarded largely as a supporting player is now entering the core spotlight: GIP. Over the past decade-plus, GLP-1 has defined the business model for weight loss drugs—high-value innovative therapeutics driven by weight reduction as the core endpoint. As the dual-agonist era advances, the role of GIP is undergoing transformation, evolving from its early perception as primarily contributing to tolerability modulation toward becoming a critical variable in metabolic architecture regulation. The significance of this shift lies not merely in adding another target, but in the broader metabolic effects associated with GIP activation. From a Single Endpoint to Multi-Parameter Synergy From an innovation trajectory standpoint, the weight-management space has already undergone a clear upgrade cycle. Single-target GLP-1 drugs, with its core value primarily reflected in weight loss and glycemic control, while effects on blood pressure, lipids, and other parameters have largely been secondary, accompanying improvements. Subsequently, dual agonists pushed weight loss magnitude closer to the ~20% range and extended benefits across certain metabolic markers, but overall market pricing has still been anchored to weight reduction and glucose lowering as the primary endpoints. Against this backdrop, BGM0504's distinguishing feature is not a breakthrough in any single metric, but rather the coordinated improvement across multiple endpoints. A 16.5 cm reduction in waist circumference suggests a direct impact on visceral fat—a core risk driver—rather than an effect limited to body weight alone. A blood pressure reduction of more than 20 mmHg, together with a target achievement rate above 90%, moves the effect from "ancillary improvement" into a clinically actionable range. A 70.7 μmol/L decrease in uric acid and a triglyceride reduction of more than 30% are approaching the magnitude typically seen with dedicated metabolic therapies. More importantly, in the context of nearly 20% weight loss, bone mineral density did not decline but instead increased, while the discontinuation rate remained at a low 0.7%. This indicates that improved efficacy was not achieved at the expense of bone loss or reduced treatment adherence. When a single drug can simultaneously improve body weight, blood pressure, blood lipids and uric acid, it demonstrates effects across multiple chronic disease populations. From Mechanism to Differentiation: The Emerging Role of GIP If the Phase III clinical data of BGM0504 represent the outcomes, the mechanism determines whether these outcomes are explainable and sustainable. Within the GLP–1 pathway, weight loss primarily stems from intake control, achieved via appetite suppression and delayed gastric emptying. Improvements in blood pressure, lipid profile, and other markers are largely secondary consequences of weight reduction. In contrast, GIP acts more as an intrinsic regulatory variable within the metabolic system. The GIP receptor is highly expressed in adipose tissue. Upon activation, it modulates adipose tissue blood flow and inflammatory status, thereby regulating fat distribution. This process not only affects body fat percentage but also drives coordinated improvements across multiple parameters—including blood lipids and blood pressure—by enhancing insulin sensitivity. From the Phase III data of BGM0504, a clear correlation can be observed with this mechanistic pathway. A 16.5 cm reduction in waist circumference indicates an impact on visceral fat, a key cardiometabolic risk factor. A 33.6% decrease in triglycerides, along with reduced LDL–C and elevated HDL–C, demonstrates favorable remodeling of lipid metabolism. A 70.7 μmol/L reduction in uric acid can be regarded as a coordinated outcome of an optimized metabolic milieu. For blood pressure, multiple factors act in concert—including reduced adipose inflammation, improved insulin resistance, and enhanced vascular endothelial function—leading to a systolic blood pressure reduction of over 22.9 mmHg and a 92.9% control rate in patients with concomitant hypertension. This pro a holistic, metabolism–driven regulatory effect. At the lipid metabolism level, GIP improves insulin sensitivity and modulates lipoprotein metabolism, thereby affecting hepatic synthesis and secretion of very-low-density lipoprotein (VLDL) while promoting triglyceride clearance in peripheral tissues. This results in a 33.6% reduction in triglycerides and optimized lipoprotein composition. Changes in uric acid metabolism largely reflect a metabolic cascade effect. In obesity and insulin resistance, renal uric acid excretion is impaired. By improving insulin sensitivity, reducing adipose inflammation, and optimizing energy metabolism, GIP helps restore uric acid excretion balance. Bone metabolism represents a distinctive feature of the GIP mechanism, supported by established human and mechanistic evidence. For instance, a study published in the Journal of Clinical Endocrinology & Metabolism demonstrated that GIP significantly inhibits bone resorption independently of insulin. GIP receptors are expressed in osteoblasts; their activation promotes bone formation and suppresses bone resorption via regulation of the RANKL/OPG pathway, thereby contributing to bone remodeling. Moreover, GIP exerts additive effects when combined with GLP-1 . Multiple reviews have identified GIP as a key regulatory hormone in the gut–bone axis, mediating both bone resorption inhibition and bone formation modulation during postprandial bone remodeling. Along the traditional single-target GLP-1 pathway, rapid weight loss is often accompanied by declines in bone mineral density, and studies show that the addition of GIP offsets this risk. Accordingly, the absence of bone mineral density loss—and even an improving trend—despite substantial weight reduction can be mechanistically explained by a combination of reduced bone resorption, enhanced bone formation, and an optimized metabolic milieu. This also provides mechanistic support for the long-term structural stability of dual-target therapies in chronic disease management. Overall, GIP is not merely an auxiliary target that amplifies weight loss. Rather, it participates in system-level regulation across multiple dimensions, including fat distribution, metabolic cross-talk, and maintenance of tissue homeostasis. When this pathway is effectively activated, a therapy's impact is no longer confined to the single endpoint of body weight, but extends across a broader set of metabolic parameters. This shift also offers a mechanistic basis for understanding BGM0504's concurrent improvements across multiple cardiometabolic indicators. BGM0504 is distinctive in that it deliberately increased the weighting of GIP at the design stage. According to a Nature - Scientific Reports publication, its dual-agonist activity is approximately three times that of tirzepatide. This difference is not merely a matter of "stronger potency"; rather, at comparable dose levels, BGM0504 appears to achieve higher GIP receptor engagement and more efficient signaling activation, materially increasing GIP's contribution to the overall pharmacology. Within this architecture, GLP-1 and GIP take on differentiated roles: GLP-1 provides the foundational effects on weight reduction and glycemic control, while GIP contributes more to fat distribution modulation, metabolic cross-talk, and tolerability optimization. From Product to Platform: GIP Is Poised to Drive a New Wave of Differentiation Once differentiation extends from mechanism into business model, shifts at the category level begin to emerge. Globally, the weight-management field is moving from single-target approaches toward multi-target combinations, along with expansion into multiple formulations and routes of administration. Beyond GLP-1 and GIP, oral options, amylin, muscle-preservation targets, and adipose signaling pathways are all becoming active frontiers of exploration. In this landscape, BrightGene Bio-Medical's strategy is closer to a platform-based approach. Building around BGM0504, the company has not only strengthened the GIP component of its mechanism, but has also advanced multiple parallel programs and modalities, including combinations of BGM0504 with amylin, an MSTN cyclic peptide, an ALK7-targeting siRNA, and several oral formulations. The goal is to assemble a systematic set of capabilities spanning adipose tissue, muscle, bone metabolism, and diverse dosing scenarios. In other words, the thesis is no longer simply to develop a single weight-loss drug, but to build a broader metabolic regulation platform. This brings us back to the original question: why was BGM0504 able to deliver consistent improvements across multiple endpoints at the same time? GIP affects multiple metabolic pathways. Clinical trials show that GLP-1 /GIP dual agonists produce effects across body weight, glycemic control, blood pressure, lipid metabolism, and uric acid levels. GIP is increasingly emerging as a key variable shaping the next phase of differentiation in this space. View original content: SOURCE BrightGene