A Phase 4, Open-Label Study of a Single Dose of Vyleesi® (Bremelanotide Injection) in Healthy, Premenopausal Lactating Female Subjects to Measure the Concentration of Bremelanotide in Breast Milk

The primary objectives of this clinical trial performed with Vyleesi (Bremelanotide Injection) are:
* to evaluate if Bremelanotide (BMT) is secreted in breast milk of lactating women treated with a single dose of BMT 1.75 mg SC.
* to measure the concentration and characterize the pharmacokinetics of BMT secreted in breast milk of lactating women treated with a single dose of BMT 1.75 mg SC.
This open-label, pharmacokinetic (PK) study will be performed in 10 healthy lactating female subjects between 10 days and 6 months post-partum (inclusive). The maximum duration of subject participation in the study will be approximately 29 days, consisting of 3-week Screening period, a 1 day treatment period, and up to a 7 day follow-up period.

开始日期2025-07-11

申办/合作机构

Cosette Pharmaceuticals, Inc.

NCT06565611

/ Active, not recruiting临床2期

A Phase II, Randomized, Double-Blind, Placebo-Controlled, Clinical Study Investigating the Safety, Tolerability, and Effectiveness of the Co-Administration of Bremelanotide With Tirzepatide (GLP-1/GIP) for the Treatment of Obesity

This is a prospective, randomized, double-blind, placebo-controlled study designed to assess the safety and efficacy of bremelanotide (BMT) used in combination with tirzepatide therapy in the treatment of obesity in subjects with a BMI ranging from 30.0 to 45.0 kg/m2 (inclusive).

开始日期2024-08-05

申办/合作机构

Palatin Technologies, Inc.

NCT05709444

/ Completed临床2期

A Phase IIb, Multicenter, Open-Label, Prospective Study of Bremelanotide in Diabetic Kidney Disease to Assess the Efficacy in Reducing Urinary Protein and Maintaining Podocyte Density and Function

This is a prospective, open-label trial to assess the efficacy of melanocortin receptor agonist bremelanotide (BMT) when administered with RAAS inhibition therapy after six months in subjects with Type II diabetic nephropathy. After six months of therapy, all subjects will remain in trial for further assessment and undergo a diagnostic renal biopsy to assess the effect of melanocortin therapy on diabetic histopathology at 12 months.

开始日期2022-12-26

申办/合作机构

Palatin Technologies, Inc.

100 项与布美诺肽相关的临床结果

登录后查看更多信息

100 项与布美诺肽相关的转化医学

登录后查看更多信息

100 项与布美诺肽相关的专利（医药）

登录后查看更多信息

项与布美诺肽相关的文献（医药）

2026-09-30·Sexual Medicine Reviews

Peptides in urology and sexual medicine: clinical effectiveness, dosing, indications, and safety: a narrative review

Review

作者: Vasylieva, Valeriia ; West, Annette ; Karpman, Edward

Abstract:

Introduction:

Peptide-based therapies are increasingly used in urology and sexual medicine, although adoption is often influenced by off-label prescribing, direct-to-consumer promotion, and limited long-term safety data. We review mechanisms, clinical evidence, dosing, safety, and regulatory status of these agents.

Methods:

A structured search of PubMed, Scopus, and Google Scholar identified studies of peptide-based therapies in sexual medicine. Search terms included Bremelanotide, Melanotan II, Kisspeptin, Oxytocin, PnPP-19, Gonadorelin and growth hormone secretagogues, including GHRP-2, GHRP-6, Ibutamoren, Ipamorelin, Tesamorelin, Sermorelin, and CJC-1295. Of 725 records, 76 studies met inclusion criteria. Findings were synthesized narratively given heterogeneity across studies.

Results:

Peptides reviewed act through diverse mechanisms, including central modulation of desire and arousal, stimulation of the hypothalamic–pituitary–gonadal and growth hormone axes, and nitric oxide–mediated effects on erectile physiology. Bremelanotide and Tesamorelin are the most clinically established agents, with defined dosing and regulatory approval for selected indications. Kisspeptin shows early promise but remains investigational. Growth hormone secretagogues reliably increase growth hormone and insulin-like growth factor 1 concentrations; however, evidence for improved sexual function, physical performance, or quality of life remains limited. Melanotan II, Ibutamoren, CJC-1295, and related agents remain accessible through unregulated markets, raising concerns about product quality, dosing variability, and incompletely characterized adverse effects. Oxytocin has biologic plausibility but limited efficacy data, whereas PnPP-19 remains preclinical. Gonadorelin was Food and Drug Administration approved but is no longer manufactured. Across peptide classes, safety data are limited by short follow-up, small samples, and incomplete assessment of cardiovascular, metabolic, and oncologic outcomes.

Discussion:

Peptide-based therapies in urology and sexual medicine show selective therapeutic potential, but most remain insufficiently validated for clinical use. Clinicians should distinguish approved therapies from investigational and nonregulated compounds and counsel patients regarding uncertain benefit, potential harm, and risks of unsupervised use. Randomized trials with standardized dosing and long-term safety assessment are needed before broader adoption.

2026-08-13·JOURNAL OF MEDICINAL CHEMISTRY

Goldilocks-Inspired Design of Mid-Size Macrocycles for Selective Targeting of Human Melanocortin Receptors

Article

作者: Tammaro, Francesco ; Grieco, Paolo ; Merlino, Francesco ; Carotenuto, Alfonso ; Santoro, Federica ; Jia, Li ; Boccino, Ida ; Thompson, Philip E.

Abstract:

The recent clinical success of macrocyclic peptides, such as bremelanotide and setmelanotide, highlights the potential of this modality as a “Goldilocks” chemical class, effectively balancing the properties of small molecules and biologics while optimizing their affinity, stability, and pharmacokinetics. Despite their potential, achieving selective MCR targeting with optimal pharmacological profiles remains challenging. Motivated by these considerations, we designed and synthesized a series of 14 macrocyclic peptide analogs (19–23-membered rings) based on MT-II, SHU-9119, and PG-901 scaffolds. Their pharmacological activities were assessed using human MC1R, MC3R, MC4R, and MC5R. The novel macrocyclic compounds FM648 and FM636 emerged as potent and selective hMC4R antagonists. Additionally, FM635 exhibited interesting agonist activity with remarkable selectivity for the same receptor. This study underscores the potential of tailored midsized macrocycles as selective MCR ligands and provides new insights into the structure–activity relationships, thereby guiding the development of therapeutic candidates for metabolic and inflammatory diseases.

2026-07-01·Journal of Minimally Invasive Gynecology

Strategies for Treating Sexual Health Concerns After Breast and Gynecologic Cancer

Review

作者: Rojas, Kristin E ; Curran, Melissa ; Mihulka, Olivia ; Narasimhan, Raksha M ; Moore, Jessica F

OBJECTIVE:

Sexual dysfunction is a common but underrecognized sequelae of breast and gynecologic cancer treatment. Many patients experience symptoms of genitourinary syndrome of menopause, including vaginal dryness, dyspareunia, and diminished sexual desire. Addressing these challenges requires a comprehensive, evidence-based approach to management.

DATA SOURCES:

A comprehensive literature search was conducted using PubMed, Google Scholar, and Scopus to identify peer-reviewed studies published within the last 30 years. The search incorporated Medical Subject Headings and keywords related to sexual dysfunction and cancer survivorship, including terms such as "sexual dysfunction," "dyspareunia," "vaginal dryness," "vaginal hormone therapy," "breast cancer survivors," and "low desire."

METHODS OF STUDY SELECTION:

Studies were included if they examined sexual dysfunction in cancer patients or survivors, were published in English, and addressed either physiological or psychological aspects of sexual health. Articles were excluded if they lacked methodological rigor. An initial screening of titles and abstracts was followed by full-text review to determine relevance and inclusion.

TABULATION:

Findings were synthesized using thematic analysis, with studies grouped by cancer type, treatment modality, and impact on sexual function. Although no formal quality assessment tool was applied, emphasis was placed on high-impact studies and comprehensive reviews published in reputable journals.

INTEGRATION AND RESULTS:

Effective management of genitourinary syndrome of menopause includes nonhormonal options such as minimizing irritants, vaginal moisturizers, lubricants, the use of dilators, and pelvic floor therapies. Local hormonal therapies may offer relief for select patients depending on the hormone sensitivity of their cancer diagnosis. For low sexual desire, psychological and pharmacological agents such as bremelanotide and flibanserin have demonstrated efficacy. Vaginal lasers and compounded hormones pose significant risks to these patient populations and should be avoided. Multidisciplinary approaches, incorporating gynecologic, psychological, and oncologic expertise, are essential for optimizing patient outcomes.

CONCLUSION:

Sexual dysfunction following breast and gynecologic cancer requires individualized, multimodal management. A combination of nonhormonal and hormonal therapies, behavioral interventions, and emerging pharmacologic treatments offers promising avenues for improving sexual health and overall quality of life in survivors. Future research should focus on the effects of specific cancer therapies on sexual health, investigate the role of biological markers and dysfunction, and refine more personalized approaches to care.

109

项与布美诺肽相关的新闻（医药）

2026-10-14

·药事纵横

“女性伟哥”的十年

被叫作“女性伟哥”的那粒粉色小药丸，最近又上了新闻。 2025年12月，美国食品药品监督管理局（FDA）批准口服药Addyi的适应证扩展，把它能治疗的群体，从绝经前女性放宽到了65岁以下的绝经后女性。Addyi的通用名是Flibanserin，早在2015年就顶着“全球首款治疗性欲低下的药物”的名头获批上市。十年过去，围绕它的争议从没停过。这次重回聚光灯下，还是那两个老问题：它到底有没有用？“性欲低下”，到底算不算一种病？ Addyi药品官网首页先把我的判断放在前面：它既没兑现“女性伟哥”的期待，也没真正回答第二个问题。上市十年，这款药销量惨淡，多数时候只存在于新闻报道和商业计划书里，活得像个都市传说。 2016年NEJM期刊发布FDA批准Flibanserin用于治疗性欲减退症一颗“无心插柳”的药这粒药的起点，其实是个意外。 2002年，德国药企勃林格殷格翰把Flibanserin当抗抑郁药来研究。临床试验做下来，抗抑郁的效果并不显著，眼看就要被放弃。可研究人员翻看受试者的自评表时，发现了一个有意思的现象：不少人写着，自己服药期间“性欲变强了”。这一下点醒了团队。Flibanserin的作用机制，是调节大脑里的血清素、多巴胺等神经递质——这些物质恰好和性欲有关。这和“伟哥”西地那非完全是两回事：后者靠扩张血管、改善勃起障碍，是“通”；前者想靠调节大脑唤醒欲望，是“调”。正如有妇产科专家反复强调的，二者原理根本不同。 Flibanserin分子式于是研究方向转向了“绝经前女性性欲低下症”（HSDD）。按当时的统计，这种“对性生活的欲望和幻想持续不足或缺失”的状态，困扰着全球5.4%到13.6%的女性，绝经前女性的发病率大约在10%。顺带说一句，“女性伟哥”这个名字其实有误导性。它并不能按需服用，得像慢性病用药一样连吃几天才能起效，和按需一粒的“伟哥”完全是两种用法。单凭这一点，后来的销量遇冷就已经写好了伏笔。 Journal of Sexual Medicine期刊发表HSDD新药临床试验研究结果两次被拒：疗效和副作用都不好看但故事没有顺着这个发现一路顺下去。 2009年，临床试验给出了一组自相矛盾的结果：电极记录仪显示，服药组和安慰剂组的性欲没有显著差异；可患者自己的评估却说，服药组“每月满意的性生活次数”多了那么一点点。建立在主观感受上的疗效，FDA不认。2010年，评审以11比0否决了上市申请。老东家心灰意冷，把药物权益转给了一家只有几十人的小公司——萌芽制药。萌芽不死心，继续扩大样本做试验，2013年再度提交申请，还是被拒。按医药行业的惯例，一个新药连续两次被FDA否决，基本可以盖棺定论了。副作用明摆着：嗜睡、疲劳、头晕、恶心、呕吐，发生率是安慰剂组的三倍多；要是喝点酒，还可能低血压、晕厥。而疗效，荟萃分析算下来，服药24周，平均每月满意的性生活次数只增加半次——还是靠患者自己“感觉”出来的。 FDA黑框警告：Addyi的低血压与晕厥风险提示让它上市的，不是疗效，是一场“平权运动” 萌芽手里几乎没有科学王牌，但它找到了另一张牌：性别权利。它盘算着：过去几十年，FDA一共批了26款治疗男性性功能障碍的药，女性的一款都没有。于是萌芽出钱赞助了一个叫Even the Score（扭转比分）的平权组织，发起“26:0”运动——在网上造势，给国会议员写信，指控FDA“性别歧视”。舆论铺天盖地。FDA被逼着出来澄清：批的26款是治疗勃起功能障碍的，不是治疗性欲低下；而男性那边，同样一款治疗性欲低下的药都没有。可道理架不住声势。2015年，萌芽第三次提交申请，FDA专家以18比6通过——附带最严重的“黑框警告”，还要求患者签署戒酒承诺。上市第二天，萌芽就把Addyi以10亿美元的价格卖给了别人。更讽刺的是，那个“义愤填膺”的平权组织，背后的金主正是萌芽自己。它曾放话要把更多女性性功能药推向市场，却在2016年悄悄关停了网站。粉色药丸的幻灭顶着“女性伟哥”的名头上架，销量却一败涂地。 2018年的数据显示，Addyi全球年销售额只有348万美元；而万艾可1998年上市当年就卖了7.88亿美元，次年破10亿，到2014年累计为辉瑞贡献了近300亿美元。原因不难懂：它不能按需服用，得连吃三天才能达到稳定浓度；副作用大得劝退，超过一成的人因受不了中途退出；收益却微乎其微。2019年获批的第二款药布美诺肽更惨——是注射剂，40%的人用药后一小时内恶心，上市后几乎被遗忘，母公司市值如今只剩3000万美元出头。更耐人寻味的是，Addyi几经转手，2018年又回到了萌芽制药手里。公司换了打法，用“性欲是女性权利”来包装营销，仍屡屡招致监管警告——产品本身没能翻身，话术倒是层出不穷。医学期刊的评论也看得透彻：即便把男女用药的“比分”追平，也弥补不了这次批准的失误——审评本该看药效，而不是看谁的声量大。蓝色和粉色小药丸的命运落差，其实藏着一根被忽略的线：男性的欲望问题，更多被当成生理问题来治；而女性的欲望，从来不是一颗药能解决的。“性欲低下”，算病吗？这个问题，学界吵了很多年，至今没有定论。反对者举出一例：美国《精神疾病诊断与统计手册》第五版，已经删除了HSDD这个诊断。有医学媒体直指，所谓“性欲低下”，是药企和医生联手把常见的性问题包装成疾病，好卖药；有美国专家说得更直白，这是“人为创造的一个能垄断的市场”。支持者则搬出世界卫生组织的医学分类和美国妇产科医师学会的意见，坚持HSDD是独立疾病，是真实存在的痛苦。国际女性性健康研究学会还专门发文回怼，说批评者“研究不足，且带明显偏见”。这场架吵不出结果。但在中国，情况更安静，也更沉默。有公立医院的科主任回忆，从医数十年，几乎没遇到过专程来看这个病的患者。有论文估计中国女性患病率或许不低，可性医学门诊鲜有开设，患者羞于开口，医生也缺系统的训练。妇产科专家段涛说得很直白：在“光吃药”之外，关系、前戏、心理干预，甚至有人愿意认真听你说，都可能比一颗药有用；而就算补充雄激素，临床上同样缺乏有效的药物手段。段涛还提了一个可参照的方向：近两年兴起的多学科联合减重门诊，会把内分泌、营养、消化、心理等不同科室拉在一起综合评估。性专科真要立起来，恐怕也得把精神、生殖、妇科、男科这几摊资源整合。只是眼下，这条路在中国还看不到尽头。值得一提的还有一点：目前仅有的两款药，都没有拿到中国药监部门的认可。Flibanserin一直没入华的动作，布美诺肽的中国独家经营权早在2017年就卖给了复星医药，复星2019年拿到临床试验注册审评受理，之后便没了下文。写在最后从2015年到现在，所谓“女性伟哥”，始终没能真正走进多数女性的生活，也没能回应她们被压抑多年的困扰。它最大的价值，或许是头一次把“女性性健康”这个长期被忽视的议题，摆到了公众面前。但当一个真实的痛苦被塞进一颗粉色药丸、被一场药企出资的“平权运动”推着上市时，我们该警惕的就不只是疗效，还有那种把痛苦打包成商品的方式。女性需要的，从来不只是“伟哥”。是正视，是理解，是有人把这件事当真。而这，显然不是光吃药能解决的。参考文献： [1] 罗澜,黄晶晶,李华芳.女性性欲评估工具及其研究应用进展[J].中国性科学,2023,32(6):152-156. [2] 罗澜,付彤,黄晶晶,等.女性性欲低下治疗药物的研发进展[J].中国性科学,2026,35(1):37-43. [3] Joffe HV, Chang C, Sewell C, Easley O, Nguyen C, Dunn S, Lehrfeld K, Lee L, Kim MJ, Slagle AF, Beitz J. FDA Approval of Flibanserin--Treating Hypoactive Sexual Desire Disorder. N Engl J Med. 2016 Jan 14;374(2):101-4. doi: 10.1056/NEJMp1513686. Epub 2015 Dec 9. PMID: 26649985. [4] ADDYI (flibanserin) tablets LABEL - Food and Drug Administration.https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/022526lbl.pdf [5] Addyi® (flibanserin) | The Little Pink Pill for HSDD, https://addyi.com/ 立即扫码加入药事纵横交流群

2026-09-30

·全球药化视野

Angew | 环肽也能口服？非天然氨基酸带来的药物设计新思路

DOI: 10.1002/anie.202523959 环肽常被视为连接小分子与生物药的一类分子：它能以较大的接触面识别蛋白，也能通过化学合成逐位改造。但环起来，并不等于就能成为好药。分子能否穿过膜、能否口服、会不会被快速降解，常常取决于环上的一个个氨基酸如何安排。这篇综述梳理了非天然氨基酸如何改变环肽的结构与成药性质，也展示了从已获批药物到新靶点探索的代表案例。接下来，我们沿着图表逐步看：哪些改造真正解决了问题，哪些结论仍需更多证据支持。目录为什么环肽需要非天然氨基酸（图1）获批药物与临床图景（图2–3；表1）把环肽调成“像药”：口服、渗透、脑暴露与稳定性（图4–7）从新靶点到复杂生物学：非天然氨基酸扩展环肽发现边界（图8–21）环肽能否补上抗体的空白（图22–25）市场、未来方向与结论1. 为什么环肽需要非天然氨基酸环肽处在小分子与生物药之间：它们能用较大的接触面识别平坦蛋白表面和蛋白—蛋白相互作用界面，也能像小分子一样通过固相合成逐位改造。但“成环”并不会自动得到好药。环化通常限制构象、提高结合亲和力与抗酶解能力；与此同时，较大的分子尺寸、多个酰胺键和高极性又会压低膜通透、口服吸收及脑暴露。本文把“非天然氨基酸”（UAA）广义定义为：经化学修饰的蛋白源氨基酸、非经典或非蛋白源氨基酸、N-甲基化残基、D-氨基酸，以及α、β、γ、δ等不同骨架长度的氨基酸。它们不只是“加一个新侧链”，还可以改变手性、主链氢键、转角偏好与环化方式。图1把设计逻辑概括为三步：线性肽可能亲和力和蛋白酶稳定性不足；环化提升构象约束；再以非天然残基精修，可在保持识别能力的同时调整通透性、代谢稳定性及PK/PD。它是概念图，不意味着每种环肽都能同时改善这些指标，真正的设计仍要逐个分子、逐个位置验证。图1｜环化与非天然残基的组合，可将构象约束转化为亲和力、稳定性和药代性质的协同优化目标。2. 获批药物与临床图景作者从获批药物回顾环肽的发展：早期天然产物和抗生素展示临床价值，1963年 Merrifield 建立固相肽合成（SPPS）后，复杂序列的可控制备与环化更可行；此后环化化学成熟、非天然氨基酸逐步商品化，环肽才得以系统进入药物发现。图2用若干节点呈现这段历史：1948年杆菌肽、1963年SPPS、环化技术兴起，以及后来setmelanotide、zilucoplan等。图2｜环肽药物由天然产物经验走向可设计、可合成、可筛选的现代药物发现。综述正文称，截至2026年有“30余种”含UAA的FDA获批宏环肽；表1逐项列出37项，图3也以37为统计总数。这个数字应理解为作者的综述纳入范围，而非只有37个临床治疗药：表中同时包含放射性诊断/治疗用示踪剂，也以星号标出已停用的peginesatide与technetium Tc-99m apcitide。作者将UAAs按宽口径处理，天然来源的复杂环肽也可能因修饰或非蛋白源残基而纳入。表1覆盖抗感染、肿瘤、内分泌、免疫、心血管及诊断等用途。从临床使用看，环肽并非单一给药路线：静脉、皮下、肌注、口服、鼻腔和局部给药均有实例。口服代表包括paritaprevir、grazoprevir、voxilaprevir、voclosporin，以及综述列出的icotrokinra；因此“肽只能注射”并不准确，但口服仍是需要针对胃肠稳定性、跨膜和首过过程共同优化的例外。表1｜FDA批准的含非天然氨基酸宏环肽：药物、靶点、适应症、给药途径及首次批准年份。图3把37项数据拆成结构、批准年代、治疗领域、给药途径和代表分子。A部分显示侧链—侧链及侧链—末端环化最常见，二硫键是重要的环化化学；单环结构占多数。B部分显示2010年代批准数量上升，疾病领域以抗菌类最多，给药途径则以静脉为主（图中53%），口服占16%。C部分以bremelanotide、setmelanotide、motixafortide、voclosporin、rezafungin及zilucoplan展示结构跨度；灰色标记为启发其开发的天然产物/模板残基，蓝色标记为优化过程中引入的残基。图内数字是本文特定纳入集合的统计，并非所有肽类药物的全球普查。图3｜获批宏环肽的构架、环化、年代、适应症与给药途径，以及代表药物和优化时引入的残基。3. 把环肽调成“像药”：口服、渗透、脑暴露与稳定性环肽药化的关键不是单独追逐高亲和力，而是同时管理靶点结合、溶解度、构象、膜通透、胃肠及血浆稳定性、清除和组织分布。原综述特别强调：影响这些性质的变量彼此牵连，单参数优化可能牺牲另一项。以下案例展示的是可用的设计手段，而不是可直接套用的通用规则。3.1 口服吸收与代谢稳定性 KRAS案例从mRNA展示筛选得到AP8784（1）起步。通过在第5位调整疏水侧链、在第11位引入N-甲基化，以及继续优化第7和第10位等结构，得到口服可用的KRAS抑制剂LUNA18（2）。图4显示细胞IC₅₀由大于20,000 nM降至1.4 nM，Caco-2表观通透系数Papp从0.02升至2.3×10⁻⁶ cm/s；动物研究在四个物种报告21%–47%的口服生物利用度。论文还报告体内肿瘤消退。这里的证据仍是临床前研究，不能由动物口服利用度推断人体疗效或临床给药方案。同图下半部分是HIV-1蛋白酶抑制剂：初始环肽对酶的IC₅₀为0.99 nM，却因细胞通透不足，抗病毒EC₅₀只有960 nM。以α-甲基脯氨酸、L-高环己基丙氨酸及Gly10→Ala等改造后，化合物4的抗病毒EC₅₀改善至37 nM，人体/大鼠肝微粒体稳定性分别为23%和63%，但大鼠口服生物利用度仍只有3.3%。其肾清除下降至8.2 mL/min/kg，带来更高的剂量校正口服暴露。这个例子提醒我们：体外靶点抑制强，未必能转化为细胞活性；而“口服可测到暴露”也不等于高生物利用度。图4｜上：AP8784经多位点优化成为LUNA18；下：HIV蛋白酶抑制剂由酶活强但细胞活性弱，转向抗病毒活性改善但口服利用度仍低。3.2 膜通透性与溶解度肽类跨膜的一个障碍，是主链NH在水中被溶剂稳定，进入膜前需要付出脱溶剂化代价。图5给出“分子内藏氢键”的思路：在环肽5中以3-Pye替代Leu₂，侧链与附近主链NH形成分子内氢键，约束构象并提高疏水性；测得pH 7.4时溶解度74 μM、Papp 14×10⁻⁶ cm/s。较大的bRo5宏环6和7则通过硫醚连接、N-烷基化与β转角偏好，形成马鞍形构象，将部分NH埋入分子内部；尽管分子量接近1000 Da、含4个氢键供体，报告的被动通透性仍可达约10×10⁻⁶ cm/s。作者同时指出，环肽构象预测和实验表征仍具挑战，因此不能只凭二维结构预测“藏氢键”一定发生。图5｜以分子内氢键和马鞍形构象降低主链极性暴露，提升大环肽通透性，并兼顾溶解度。3.3 血脑屏障通透脑暴露案例以LMP2抑制剂DB-60（8）为起点。对脯氨酸位置引入反式氟取代并配合其他结构调整后，化合物9的LMP2 IC₅₀从184.1 nM改善至87 nM，半衰期从1.35 min延长至38.4 min；大鼠口服生物利用度为9.8%。图6标示100 mg/kg下脑内LMP2抑制65%；正文还报告静脉给药24小时后，40与100 mg/kg剂量分别仍有39%和65%抑制。对接模型推测氟取代可能作为氢键受体，与靶蛋白His114/His116相互作用。脑内靶点占有/抑制及高Papp支持其具有脑暴露潜力，但它是临床前候选，不代表已证明阿尔茨海默病治疗效果。图6｜DB-60经氟代及配套改造后，LMP2活性、体内半衰期、口服暴露及脑内靶点抑制均有改善。3.4 抗蛋白酶降解 IFNGR1拮抗环肽说明，骨架和手性可以直接改变血清稳定性。N端氯乙酰-D-酪氨酸与C端D-半胱氨酸形成硫醚环化，配合D-α、β及γ氨基酸残基；β¹基序对抑制活性和稳定性都重要。将Arg改成鸟氨酸（Orn），并改变环内γ氨基酸后，两个代表分子的血清半衰期达到33和49小时，IFNGR1结合Kd分别11和12 nM；图示细胞IC₅₀数值为3.5 mM与0.75 mM。正文另报告优化前后活性及血清稳定性倍数，提醒读者要注意实验条件和单位，不能把结合Kd与细胞功能IC₅₀直接横向比较。图7｜D、β和γ氨基酸及Orn取代协同改善IFNGR1环肽稳定性，并维持纳摩尔级结合。4. 从新靶点到复杂生物学：非天然氨基酸扩展环肽发现边界本节案例来自不同筛选平台和疾病领域。共同点不是某一种UAA“万能”，而是非天然残基扩大了文库化学空间，并在命中后提供可调整的构象、蛋白酶切位点和靶点接触面。4.1 靶向LPS转运的新型抗生素 Zosurabalpin（图8）源自约44,985个宏环肽的全细胞表型筛选，目标是鲍曼不动杆菌，尤其碳青霉烯耐药菌株（CRAB）。初始先导RO7036668经脂溶性优化后有很强体外活性，但静脉给药动物出现高死亡率，说明体外MIC不足以保障体内可用性。之后利用两性离子设计降低血浆聚集/沉淀，得到zosurabalpin；综述列出其对A. baumannii的MIC约0.25 mg/L，并指出其通过LptB₂FGC转运系统阻断脂多糖运输，破坏革兰阴性菌外膜。L-鸟氨酸与L-N-甲基色氨酸是该骨架的重要设计元素。临床开发阶段与获批治疗仍须区分；本文引用的是临床阶段资料。图8｜由全细胞筛选命中物优化而来的两性离子环肽，靶向LPS转运复合体；图中对比先导与zosurabalpin。4.2 BamA抑制剂：利用非天然残基识别膜蛋白 BamA参与革兰阴性菌外膜蛋白折叠与插入，是结构复杂、较难用常规小分子占据的靶点。PDPS平台得到CP1、CP2、CP3等含多个UAA的宏环肽，对E. coli BamA的Kd为2.0–6.6 nM；对E. coli BamA101菌株的MIC为6.3–12.5 μM。共晶结构显示它们进入β桶腔内、与darobactin的结合位点不同。CP3的PeGly6可与Q466形成氢键，CP2中的Tic与T514发生极性相互作用。效力主要在大肠杆菌显示，且有物种选择性；这是先导发现证据，不等于已有广谱抗菌药。图9｜CP1–CP3利用PeGly、Tic等残基占据BamA β桶内独特口袋；结合强并不意味着跨菌种广谱。4.3 肾纤维化：用成环和订书肽提高暴露从油菜籽蛋白来源的线性肽DR8，到引入α-(4-戊烯基)-Ala的DR3penA，抗纤维化活性有所改善，但后者体内半衰期仍只有0.19小时。研究者根据螺旋构象假设，用烃链订书、半胱氨酸订书及头尾环化强化构象；随后在蛋白酶切位点引入UAA，并连接适当脂肪酸。图10的肽27在输尿管梗阻小鼠模型中，0.05 mg/kg腹腔给药显示抗纤维化作用，半衰期较DR3penA提高5.68倍。结果是动物模型证据；模型中纤维化指标改善不能替代人类肾病疗效验证。图10｜DR8到DR3penA再到订书/环化肽27：稳定性、系统暴露与小鼠肾纤维化药效逐步优化。4.4 May1抑制剂：面向隐球菌的口服先导隐球菌分泌的May1蛋白酶有助于其在低pH环境生存并参与毒力。苯基他汀衍生物12先显示选择性；随后加入非天然残基并进行树脂上环化，得到13与14。两者对May1的Ki分别为400和180 pM。化合物14含3-吡啶丙氨酸，口服生物利用度12.5%、口服给药半衰期83.7分钟；13的数据为6.0%和42.4分钟，且小鼠实验中出现高发病/严重不良表现。图11强调，筛选中要同时考虑效价、选择性和耐受性，而非只挑Ki最小者。图11｜环化与侧链UAA将May1抑制从纳摩尔提升到亚纳摩尔；13与14的动物耐受性和口服PK不同。4.5 γ氨基酸环肽抑制SARS-CoV-2主蛋白酶 RaPID筛选得到含γ氨基酸的非共价Mpro抑制剂GM4，IC₅₀为50 nM、Kd为5.2 nM；cis-3-氨基环丁烷甲酸这一γ残基使其蛋白酶稳定性较Ala类似物提高12倍。将His3替换为Gln后得到GM4H3Q，IC₅₀降至10 nM、Kd为0.86 nM，稳定性大致保持。图12和晶体/切割位点分析支持UAA参与构象与酶切抗性。这里展示的是分子与体外酶学证据，不是抗病毒临床疗效。图12｜γ氨基酸提高Mpro环肽的构象与蛋白酶稳定性；His→Gln进一步改善体外抑制效价。4.6 NTS2选择性镇痛肽神经降压素片段NT(8–13)可在疼痛模型中发挥作用，但不能区分NTS1与NTS2。通过序列扫描、宏环化和UAA/连接臂优化，研究者提高NTS2选择性，并延长血浆半衰期。最终候选MD01-67对NTS2的Ki为2.9 nM，对NTS1大于100 μM，选择性超过30,000倍；其结构以γ-支链环脂肪族氨基酸调节结合，并用烯丙基甘氨酸实现侧链—侧链环化。作者报告其为无阿片类选择性镇痛先导，并可增强吗啡作用；动物药效不能等同于已证实的人体镇痛或减少阿片用量。图13｜从无亚型选择性的神经降压素片段，优化出高度偏向NTS2的宏环肽MD01-67。4.7 口服凝血酶抑制剂凝血酶环肽的早期骨架含β-高脯氨酸及硫醚/砜连接，Ki为82 nM，但易被氧化。以烃链连接后，化合物17稳定性和Ki（50 nM）改善，然而大鼠口服生物利用度仅4.5%。再把易氧化的氯噻吩换成4-氯苯基，得到18：Ki为65 nM、大鼠口服生物利用度提高到18.4%，PAMPA通透性与微粒体稳定性也改善。图14体现了一个常见事实：解决代谢脆弱点，并不自动解决口服吸收；多个位点需要联合迭代。图14｜先改善凝血酶环肽氧化稳定性，再调整末端芳基，口服利用度由4.5%升至18.4%。4.8 双环肽调节Gαi蛋白 Gαi难以被传统配体调节。线性肽GPM-1连接细胞穿透肽后可进入细胞；进一步环化得到GPM-1d，稳定性与效力优于线性形式。随后双环文库筛选发现GPM-3可结合Gαi的α螺旋结构域与switch III区，表现为GAP调节；GPM-2偏好GDP结合态，呈GEF样作用。UAA参与疏水接触，双环约束帮助维持细胞内作用。图15是作用模式与结构示意，细胞穿透肽是递送设计的一部分；这些结果不代表已有体内疾病疗法。图15｜从线性、单环到双环GPM肽，利用非天然残基和构象限制调节Gαi不同核苷酸状态。4.9 镜像D肽抑制MMP7 MI-RaPID筛选产生含环状β氨基酸的镜像肽D′20；其全D构型并含(1R,2R)-2-氨基环己烷甲酸和硫醚大环。它对人MMP7的IC₅₀为90 nM，对其他MMP亚型有选择性；在人血清中至少24小时稳定，在模拟胃液/肠液中12小时保持稳定。胰腺癌CFPAC-1细胞迁移抑制IC₅₀约1 μM，且未观察到明显细胞毒性。图16的镜像策略借助D构型降低常见蛋白酶识别，但尚需继续验证体内分布、免疫性质及疾病模型效果。图16｜D型环肽及环状β残基提高蛋白酶抗性，同时维持对MMP7的选择性抑制。4.10 镜像D肽靶向MDM2与CHIP 镜像噬菌体展示（MIPD）先制备靶蛋白D型镜像，再筛选与之结合的D肽，最后合成正常手性目标分子对应的候选肽。该策略分别为MDM2与E3泛素连接酶CHIP找到硫醚订书宏环。D-H101、D-H102、D-H103识别MDM2疏水口袋；D-H201至D-H203通过疏水残基和末端羧酸与CHIP相互作用。图17列出肽序列及结合/细胞数据。D构型可增加代谢稳定性，但靶点结合本身不等同于已证明的肿瘤抑制效果。图17｜镜像筛选拓展了D型宏环肽空间，获得可结合MDM2与CHIP的候选分子。4.11 靶向泛素链的细胞可渗透环肽针对Lys48连接多聚泛素链的环肽可能干预泛素—蛋白酶体系统。RaPID筛选得到细胞可渗透的Ub4iX，可抑制癌细胞生长并诱导凋亡；Ub4a对K48四泛素的Kd为9 nM，体外抑制去泛素化与蛋白酶体降解。经N-甲基化、D残基及脂溶性Aoc等优化后，血浆半衰期达到60小时；小鼠模型中观察到肿瘤生长抑制。图18并列展示Ub4iX、Ub4a与亲和力较弱的Ub4e。细胞渗透和动物模型的抗肿瘤信号值得关注，但临床可用性、安全窗及选择性仍需研究。图18｜K48多聚泛素识别肽通过结构优化获得纳摩尔结合、细胞作用与较长血浆半衰期。4.12 DOR激动剂：在酪氨酸上引入Dmt 在环状脑啡肽DPDE中，将N端Tyr换成2′,6′-二甲基酪氨酸（Dmt），可增强受体结合：对δ阿片受体DOR的Ki提升约10倍至1.8 nM，对μ受体MOR提升约35倍至58.3 nM；小鼠输精管实验中DOR激动效力提高86倍，外周给药小鼠也见镇痛作用。图19的关键是一个位置明确的侧链修饰，就改变了受体亲和力与功能。动物镇痛及受体数据不能回答长期安全性、耐受和人体有效剂量。图19｜Dmt替代Tyr后，脑啡肽类环肽对DOR/MOR的亲和力和外周镇痛表现改变。4.13 Endomorphin-2衍生混合阿片受体激动剂内源性endomorphin-2（EM-2）对MOR有选择性，但容易代谢。引入多个UAA并环化得到化合物19后，体外对MOR、κ受体KOR及DOR均有活性：IC₅₀分别0.49、0.30、11.2 nM；在小鼠中腹腔给药10 mg/kg显示镇痛，作者认为其有脑内暴露迹象。图20同时提示它从选择性MOR配体转为MOR/KOR混合激动剂。受体谱拓宽既可能带来疗效，也可能增加中枢副作用，需通过系统安全性研究判断。图20｜EM-2环化并引入UAA后成为混合MOR/KOR激动剂；结构优化伴随药理选择性的改变。4.14 Daptomycin类似物Kynomycin Daptomycin是临床使用的环脂肽，耐药肠球菌推动了类似物研究。对其非天然氨基酸犬尿氨酸（Kyn）进行N-甲基化得到kynomycin；图21比较二者结构与临床菌株MIC。Kynomycin对MRSA和金黄色葡萄球菌的MIC为0.25 μg/mL（daptomycin为0.5），对肠球菌类也有改善；动物感染模型中疗效优于daptomycin且毒性较低，溶血测试至320 μg/mL未见明显溶血。机制实验支持其更强扰动细菌膜。需要注意，图中灰色标记指出天然产物本身已含UAA；改造是在既有特殊残基上进一步N-甲基化。图21｜对daptomycin中Kyn残基进一步N-甲基化得到kynomycin，体外MIC及动物感染数据有所改善。5. 环肽能否补上抗体的空白宏环肽可能识别抗体常面对的蛋白—蛋白界面，同时具有较小尺寸、化学合成和位点改造优势。但“可作为替代”是药物发现路径，不表示已普遍取代单克隆抗体。图22–25展示了从临床验证药物到早期候选的不同成熟度。5.1 IL-23受体拮抗剂：icotrokinra Icotrokinra（JNJ-77242113/JNJ-2113）是含多种UAA的大型宏环肽，结合IL-23受体胞外域的Kd为7.1 pM，抑制IL-23信号的IC₅₀为5.6 pM，并保留对IL-12信号的选择性。综述报告其在中重度斑块型银屑病临床试验达到主要疗效终点，并描述为已获FDA批准；图22强调其口服潜力与极高亲和力。该案例说明宏环肽可以口服并作用于细胞外蛋白互作，但高结合亲和力只是完整临床药理的一部分。图22｜Icotrokinra以宏环肽阻断IL-23R信号，具有皮摩尔级结合与选择性，并展示口服环肽临床路线。5.2 PD-L1抑制剂BMS-986238 第一代PD-L1宏环肽BMS-986189半衰期较短。对溶剂暴露区域进行脂肪酸/白蛋白结合优化，得到第二代BMS-986238；其在大鼠和食蟹猴中的半衰期超过19小时，具有低皮摩尔级结合能力。制剂研究提示可能适合口服，但论文将其描述为临床试验中的候选。图23中脂质/亲水连接臂是提升循环暴露的设计重点；目前不应把动物PK或早期开发状态写成已证实口服抗肿瘤疗效。图23｜脂肪酸与亲水连接臂提高PD-L1宏环肽血清蛋白结合和动物半衰期。5.3 CD47–SIRPα免疫检查点 CD47在肿瘤细胞上高表达，与髓系细胞SIRPα结合后抑制吞噬。抗体阻断可能因红细胞也表达CD47而引起非特异清除与贫血。RaPID筛选得到15残基环肽D4-2，结合小鼠SIRPα免疫球蛋白样V结构域（Kd 8.22 nM），通过变构改变SIRPα构象、削弱CD47互作。D4-2在体外促进巨噬细胞吞噬肿瘤细胞，并增强rituximab、TA-99等抗体效应。图24上半部分为D4-2；“潜在更安全”是作者对选择性策略的展望，不能代替临床安全性数据。5.4 Zilucoplan：补体C5抑制图24下半部分是已获批用于全身型重症肌无力的皮下注射宏环肽zilucoplan。它含环己基甘氨酸、氮杂色氨酸、叔丁基甘氨酸、N-甲基天冬氨酸及PEG连接的C16脂质尾。对人C5的Kd为0.43 nM，抑制补体介导溶血的IC₅₀为3.2 nM，并可变构阻止C5裂解和膜攻击复合体形成；在体外保留对eculizumab耐药C5变体R885H的活性。重建基底膜模型提示其组织通透性高于eculizumab类似物。zilucoplan是这一综述中UAA环肽临床转化的代表；不同实验模型中的通透性比较不能泛化为所有组织或所有抗体。图24｜上：变构调节CD47–SIRPα轴的D4-2；下：含脂质尾的C5抑制剂zilucoplan。5.5 Nectin-4双环肽—毒素偶联物BT-8009 噬菌体展示得到识别肿瘤靶点Nectin-4的双环肽后，研究者通过亲水UAA（D-Asp、反式羟脯氨酸、Nal、hArg等）优化稳定性，再连接可裂解连接臂和细胞毒载荷MMAE，形成BT-8009（zelenectide pevedotin）。结合Kd约2.5 nM，动物研究显示肿瘤活性；I/II期临床研究报告尿路上皮癌患者中的初步疗效与可接受安全性。图25上半展示靶向肽、间隔臂及MMAE载荷。它是双环肽偶联药物的临床探索，不是已获批产品。5.6 口服PCSK9抑制剂MK-0616 PCSK9抑制可减少LDL受体降解，传统获批方案以注射抗体或核酸药物为主。mRNA展示筛选与结构指导优化得到口服宏环肽MK-0616（enlicitide），含5-氟色氨酸、羟脯氨酸、O-甲基酪氨酸、α-甲基脯氨酸等UAA，对PCSK9体外Ki为5 pM。临床前研究显示口服可用并推进临床；综述撰写时描述为III期开发。图25下半展示完整环肽结构。超高亲和力不自动等于临床心血管获益，关键仍在长期LDL-C降低、安全性和结局证据。图25｜上：Nectin-4双环肽连接MMAE载荷；下：含多种UAA、具口服开发潜力的PCSK9抑制剂MK-0616。6. 市场、未来方向与结论原综述的市场部分引用外部商业报告：估算2024年全球肽类药物市场约491.3亿美元，并预测2034年达到837.5亿美元。该预测涵盖广义肽类药物，不等于非天然氨基酸宏环肽的独立市场规模；市场估值与远期预测随口径和时间变化，本文只将其作为原文背景，不视为实时更新数据。综述列举semaglutide、tirzepatide及octreotide等销售额，也属于作者采用的2024年历史资料。未来主要挑战包括：如何在高亲和力之外同步优化口服吸收、脑渗透、蛋白酶稳定性和全身分布；如何理解细胞摄取与内体逃逸；如何更可靠地预测和测量大环构象；以及如何让平台筛选覆盖更广的UAA化学空间。作者看好mRNA展示、噬菌体展示、DNA编码库、单珠单化合物筛选、合成生物学与AI设计的结合，并认为二硫醚等温和环化化学可能继续扩展。综观全文，非天然氨基酸的价值不在“越多越好”，而在于把结构变化精准放在需要解决的瓶颈上：一个D残基可抵抗蛋白酶；一个N-甲基或β/γ残基可改变主链构象；一个疏水侧链或脂质尾可改变靶点接触、膜分配或循环时间。成功候选往往来自筛选、结构信息、化学合成和PK/PD数据的多轮迭代。环肽能触达许多传统小分子难以覆盖的蛋白界面，但每个案例的证据阶段不同，体外亲和力、动物口服暴露、临床试验和获批疗效必须严格区分。

2026-09-28

·PRNewswire

Palatin Reports Fiscal Year 2026 Financial Results and Provides Business Update

Programs are focused on rare obesity disorders associated with the melanocortin 4 receptor (MC4R) pathway, including hypothalamic obesity, Prader-Willi syndrome and Bardet-Biedl syndrome Once-weekly injectable MC4R selective peptide agonist Phase 1 SAD/MAD study targeted to initiate in the first half of calendar 2027, with initial data targeted in the second half of 2027 Oral MC4R selective agonist Phase 1 SAD/MAD study targeted to initiate in the second half of calendar 2027, with initial data targeted in the first half of 2028 Multiple lipidated and non-lipidated peptide compounds demonstrated potent MC4R agonist activity but are not agonists at melanocortin 1 receptor (MC1R), supporting the potential to minimize or eliminate MC1R-mediated hyperpigmentation Fiscal 2026 collaboration and license revenue totaled $13.2 million, with approximately $9.4 million related to Boehringer Ingelheim and $3.8 million of non-cash license revenue under the Altanispac Labs agreement Cash and cash equivalents were $7.5 million as of June 30, 2026; additional funding will be required to continue advancing development programs and fund operations Conference call and webcast scheduled for September 28, 2026, at 11:00 a.m. ET PRINCETON, N.J., Sept. 28, 2026 /PRNewswire/ -- Palatin Technologies, Inc. (Nasdaq: PTN), a biopharmaceutical company developing medicines that target the melanocortin receptor ("MCR") system, today reported financial results for the fiscal year ended June 30, 2026 and provided an update on its MC4R-focused obesity development programs and partnering activities. "MC4R agonism is now clinically and commercially validated in multiple rare and syndromic obesity disorders, establishing a strong foundation for the development of next-generation therapies," said Carl Spana, Ph.D., President and Chief Executive Officer of Palatin Technologies. "While currently available and emerging therapies have demonstrated meaningful efficacy, gastrointestinal adverse events and hyperpigmentation remain important challenges for patients requiring long-term treatment. Our objective is to develop MC4R therapies that deliver comparable or greater efficacy with improved tolerability, little to no hyperpigmentation, and product profiles suitable for lifelong use." "We are advancing two complementary peptide series, non-lipidated PL1000 and lipidated PL2000, with tested compounds from both demonstrating potent MC4R agonist activity and not acting as agonists at MC1R. These findings support our strategy to minimize or potentially eliminate MC1R-mediated hyperpigmentation. Combined with our work to improve gastrointestinal tolerability, develop a long-acting injectable therapy and advance our oral small-molecule program, we believe we are building a differentiated portfolio for patients with rare and syndromic obesity disorders," continued Dr. Spana. Obesity Program Update Palatin is advancing three distinct and complementary treatment approaches to developing selective MC4R agonists for rare and syndromic obesity disorders: a lipidated peptide program, a non-lipidated peptide program, and an oral small-molecule program. The programs are being designed around a common target product profile of meaningful efficacy, improved tolerability, little to no hyperpigmentation and dosing profiles suitable for long-term treatment. Initial clinical development is planned in hypothalamic obesity ("HO"), Prader-Willi syndrome ("PWS") and Bardet-Biedl syndrome ("BBS"), with potential application to other rare MC4R pathway disorders. The Company is progressing these programs toward clinical development, with IND-enabling and CMC activities ongoing for the lead lipidated peptide candidate, controlled-release formulation optimization for the non-lipidated candidate, and continued preclinical optimization of the oral small-molecule program. Planned development activities, clinical studies and associated milestones remain subject to the availability of appropriate funding. Next-Generation Peptide MC4R Selective Agonists Palatin is advancing two complementary selective MC4R peptide series: non-lipidated PL1000 and lipidated PL2000, with the objective of developing long-acting subcutaneous therapies suitable for chronic treatment. Palatin's lead lipidated MC4R peptide development candidate has demonstrated significant reductions in food intake and body weight with once-weekly subcutaneous dosing in a diet-induced obese mouse model. Preclinical pharmacokinetic data support the potential for once-weekly or less frequent dosing in humans. IND-enabling and CMC activities are ongoing for the lead lipidated peptide candidate in preparation for planned first-in-human clinical development. For its lead PL1000 non-lipidated peptide candidate, Palatin has established the feasibility of once-weekly subcutaneous dosing and is working to optimize a controlled-release formulation. Tested compounds from both peptide series have demonstrated potent MC4R agonist activity and are not agonists at MC1R, supporting Palatin's objective to minimize or potentially eliminate MC1R-mediated hyperpigmentation. A Phase 1 SAD/MAD study of the lead lipidated peptide candidate is targeted to initiate in the first half of calendar 2027, with initial data targeted in the second half of calendar 2027. Oral MC4R Selective Agonists Palatin is developing oral small-molecule MC4R selective agonists as a third and complementary treatment approach, building on learnings from its earlier drug candidate, PL7737, and utilizing multiple drug-design approaches, including AI and ML tools. Preclinical work has identified candidates with improved potency and MC4R selectivity relative to earlier compounds, along with favorable oral bioavailability. Palatin's objective is to develop an oral MC4R agonist capable of delivering comparable or greater efficacy with improved tolerability compared with emerging oral MC4R therapies, while limiting or avoiding MC1R agonism to minimize or eliminate hyperpigmentation. A Phase 1 SAD/MAD study is targeted to initiate in the second half of calendar 2027, with initial Phase 1 data targeted in the first half of calendar 2028. Partnering and Out-Licensing Update Retinal Diseases – Boehringer Ingelheim Palatin and Boehringer Ingelheim have a research collaboration and license agreement covering proprietary MCR-targeted compounds for retinal diseases. Palatin recognized approximately $9.4 million in collaboration and license revenue related to the agreement during fiscal 2026. Palatin remains eligible for success-based development, regulatory and commercial milestone payments and tiered royalties on net sales of licensed products. Palatin conducts collaborative research and development activities, with approved costs reimbursed by Boehringer Ingelheim. PL9643 – Dry Eye Disease Palatin has an exclusive sublicense agreement with Altanispac Labs for PL9643 in dry eye disease. Palatin recognized approximately $3.8 million in fiscal 2026 license revenue under the agreement in the form of non-cash debt cancellation. Palatin remains eligible for future payments and tiered royalties under the agreement. PL8177 – Ulcerative Colitis Palatin has reported positive Phase 2 proof-of-concept results for PL8177 in ulcerative colitis. PL8177 is available for partnering or out-licensing, and strategic discussions are ongoing. Diabetic Nephropathy – MCR Agonist Palatin has reported positive Phase 2 open-label results with an MCR agonist in diabetic nephropathy. The program is available for partnering or out-licensing, and strategic discussions are ongoing. Fiscal Fourth Quarter and Year Ended June 30, 2026 Financial Results Revenue For the fiscal fourth quarter ended June 30, 2026, Palatin recognized approximately $0.3 million in collaboration and license revenue, compared with no revenue for the comparable prior-year period. For the fiscal year 2026, Palatin recognized $13.2 million in collaboration and license revenue, compared with no revenue for fiscal year 2025. The collaboration and license revenue recognized was related to the Boehringer Ingelheim and Altanispac agreements. Operating Expenses Total operating expenses were approximately $4.7 million for the fiscal fourth quarter ended June 30, 2026, compared with approximately $2.3 million for the comparable prior-year period, which included gains related to Vyleesi and purchase commitments. For fiscal year 2026, total operating expenses were $21.9 million compared with $17.5 million for fiscal year 2025, which included a $3.1 million gain on the sale of Vyleesi and a $2.1 million gain on purchase commitments. Research and development expenses were approximately $2.0 million for both the fiscal fourth quarter ended June 30, 2026 and the comparable prior-year period. For fiscal year 2026, research and development expenses were $12.4 million compared with $14.9 million for fiscal year 2025. The year-over-year decrease was primarily attributable to lower expenses related to the timing of certain activities on the Company's MC4R programs. General and administrative expenses were approximately $2.7 million for the fiscal fourth quarter ended June 30, 2026, compared with approximately $2.6 million for the comparable prior-year period. For fiscal year 2026, general and administrative expenses were $9.5 million compared with $7.8 million for fiscal year 2025. The year-over-year increase was primarily attributable to higher professional fees. Net Loss For the fiscal fourth quarter ended June 30, 2026, Palatin reported a net loss of $4.4 million, or $(1.11) per basic and diluted common share, compared with a net loss of $2.2 million, or $(2.73) per basic and diluted common share for the comparable prior-year period. The increase in net loss was primarily attributable to gains related to Vyleesi and purchase commitments that reduced operating expenses for the fourth quarter ended June 30, 2025. For fiscal year 2026, Palatin reported a net loss of $8.4 million, or $(2.96) per basic and diluted common share, compared with a net loss of $17.3 million, or $(32.15) per basic and diluted common share for fiscal year 2025. The reduced fiscal-year net loss was primarily attributable to collaboration and license revenue recognized during fiscal year 2026, offset by gains related to Vyleesi and purchase commitments that reduced operating expenses for fiscal year 2025. Cash Flows Net cash used in operating activities was $13.5 million for fiscal year 2026 compared with $21.3 million for fiscal year 2025. The decrease was primarily attributable to the lower net loss resulting from collaboration and license revenue under the Boehringer Ingelheim and Altanispac agreements. Net cash provided by financing activities was $18.5 million during fiscal year 2026, consisting primarily of approximately $16.9 million in net proceeds from sales of common stock and warrants and $1.6 million from warrant exercises. Net cash provided by financing activities during fiscal year 2025 was $11.2 million, consisting primarily of approximately $8.0 million in net proceeds from sales of common stock and warrants and $3.4 million from warrant exercises offset by approximately $0.2 million of cash payments for lease and tax obligations. Cash Position As of June 30, 2026, Palatin had $7.5 million in cash and cash equivalents, compared with $2.6 million as of June 30, 2025. Current liabilities were approximately $1.8 million as of June 30, 2026. Based on our cash and cash equivalents as of June 30, 2026, and our current operating and development plans, including our ability to reduce or delay certain expenditures within management's control, we do not expect our existing cash and cash equivalents to be sufficient to fund our operations for at least twelve months following the issuance of these financial statements. We will require additional financing to continue advancing our development programs and fund our operations. Although we intend to pursue additional capital through equity financings, collaboration arrangements and other potential sources, there can be no assurance that financing will be available when needed or on acceptable terms. Accordingly, substantial doubt exists about our ability to continue as a going concern. Conference Call / Webcast Palatin will host a conference call and audio webcast on September 28, 2026, at 11:00 a.m. ET to discuss fiscal 2026 financial results and provide an update on corporate and development activities. To listen to the live conference call, dial 1-888-506-0062 (US) or 1-973-528-0011 (International), Participant Access Code: 115353. The audio webcast and replay can be accessed by logging on to the "Investor-Webcasts" section of Palatin's website at . A telephone and audio webcast replay will be available one hour after the completion of the call. To access the telephone replay, dial 1-877-481-4010 (US) or 1-919-882-2331 (International), Replay Passcode 54564. The webcast and telephone replay will be available through October 12, 2026. Role of MC4R Agonists in Obesity Hypothalamic neurons expressing the melanocortin-4 receptor ("MC4R") play a central role in regulating stored energy, food intake and body weight. When MC4R pathway signaling is impaired, patients can experience severe hunger, reduced energy expenditure and early-onset or severe obesity. MC4R agonism represents a clinically validated therapeutic approach for obesity disorders driven by dysfunction of the melanocortin pathway. About Hypothalamic Obesity Hypothalamic obesity (HO) is a rare and severe form of obesity caused by dysfunction or damage to the hypothalamus, the region of the brain that regulates appetite, satiety, and energy balance. HO can occur as an acquired condition, most commonly after surgery or radiation therapy for brain tumors such as craniopharyngioma, or as a congenital disorder associated with genetic syndromes and developmental abnormalities affecting hypothalamic function. Individuals with HO typically experience rapid weight gain, intense hunger, and serious metabolic problems that are resistant to conventional diet, exercise, and behavioral interventions. Although therapeutic options have recently emerged, HO remains a condition with significant unmet medical need, particularly with respect to long-term efficacy, tolerability, and patient management. About Prader-Willi Syndrome Prader-Willi syndrome (PWS) is a rare, complex genetic neurodevelopmental disorder caused by the loss of function of specific genes on chromosome 15. The condition is characterized by hyperphagia, impaired satiety, developmental delays, reduced muscle tone, endocrine abnormalities, and behavioral challenges. Individuals with PWS typically develop an intense and persistent drive to eat, beginning in early childhood, which can lead to severe obesity and related metabolic complications if not strictly managed. Current treatment approaches focus primarily on symptom management, including nutritional supervision, behavioral interventions, and growth hormone therapy. While new drug therapies are emerging, there remains significant unmet need, particularly in addressing hyperphagia and improving long-term tolerability and patient adherence. About Bardet-Biedl Syndrome Bardet-Biedl syndrome (BBS) is a rare genetic disorder characterized by early-onset obesity, hyperphagia, retinal degeneration, renal abnormalities, and developmental and cognitive impairment. Obesity in BBS is driven, in part, by dysfunction in the melanocortin signaling pathway, leading to impaired satiety and increased food intake. Individuals with BBS often experience significant, early weight gain and associated metabolic complications that are difficult to manage with conventional interventions. While targeted therapies have recently been approved, BBS remains a serious and lifelong condition with ongoing unmet need, particularly with respect to treatment tolerability, durability of treatment benefit, and overall patient quality of life. About Melanocortin Receptor Agonists The melanocortin receptor ("MCR") system is involved in the regulation of metabolism, food intake, inflammation, immune responses and sexual function. There are five melanocortin receptors, MC1R through MC5R. Modulation of these receptors through receptor-specific agonists or antagonists can produce medically significant pharmacological effects. About Palatin Palatin is a biopharmaceutical company developing first-in-class medicines based on peptide and small-molecule compounds that modulate the activity of the melanocortin receptor system. Palatin's principal strategic development focus is advancing selective MC4R agonists for rare obesity disorders, while utilizing collaborations, licensing arrangements and strategic partnerships to advance other MCR-based programs and generate potential milestone and royalty economics. For more information, visit the Company's website at . Forward Looking Statements. Statements in this press release that are not historical facts, including statements about future expectations of Palatin Technologies, Inc., such as statements about Palatin products in development, clinical trial timing and results, potential actions by regulatory agencies, regulatory plans, development programs, proposed indications for product candidates, financing and cash runway, and market potential for product candidates, are "forward-looking statements" within the meaning of Section 27A of the Securities Act of 1933, Section 21E of the Securities Exchange Act of 1934 and the Private Securities Litigation Reform Act of 1995. Palatin intends that such forward-looking statements be subject to the safe harbors created thereby. Such forward-looking statements involve known and unknown risks, uncertainties and other factors that could cause Palatin's actual results to be materially different from its historical results or from any results expressed or implied by such forward-looking statements. Palatin's actual results may differ materially from those discussed in the forward-looking statements for reasons including, but not limited to, results of preclinical studies and clinical trials, regulatory actions by the FDA and other regulatory authorities, Palatin's ability to fund development of its technology and establish and successfully complete clinical trials, the length of time and cost required to complete clinical trials and submit applications for regulatory approvals, products developed by competing pharmaceutical, biopharmaceutical and biotechnology companies, commercial acceptance of Palatin's products, and other factors discussed in Palatin's periodic filings with the Securities and Exchange Commission. Palatin undertakes no obligation to update forward-looking statements except as required by law. SOURCE Palatin Technologies, Inc. 21% more press release views with Request a Demo

引进/卖出财报临床结果

100 项与布美诺肽相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D06569 D11629	布美诺肽	G02CX05 G	DB11653

研发状态

批准上市

10 条最早获批的记录,

后查看更多信息

适应症	国家/地区	公司	日期
心理性性功能障碍	美国	Cosette Pharmaceuticals, Inc.	2019-06-21

未上市

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
女性性功能障碍	临床3期	加拿大	Palatin Technologies, Inc.	2014-12-31
肥胖	临床2期	美国	Palatin Technologies, Inc.	2024-08-05
糖尿病肾病	临床2期	美国	Palatin Technologies, Inc.	2022-12-26
勃起功能障碍	临床2期	美国	Palatin Technologies, Inc.	-
性欲障碍 NOS	临床1期	中国	Palatin Technologies, Inc.	2020-10-16
性欲障碍 NOS	临床1期	中国	上海复星医药产业发展有限公司	2020-10-16
出血性休克	临床前	美国	Palatin Technologies, Inc.	-
血管疾病	临床前	美国	Palatin Technologies, Inc.	-

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT06565611 (BMT-801, PRNewswire) 人工标引	临床2期	肥胖	-	bremelanotide + tirzepatide	選範夢艱衊鹽淵鑰衊願(蓋鹽壓鏇鹽壓積選蓋選) = 壓積鏇窪構繭鏇網襯齋廠顧構選鏇獵窪糧積製 (觸範顧鹽範襯製衊築構 ) 更多	积极	2025-04-17
				Bremelanotide alone	選範夢艱衊鹽淵鑰衊願(蓋鹽壓鏇鹽壓積選蓋選) = 襯繭壓襯選醖獵觸襯遞廠顧構選鏇獵窪糧積製 (觸範顧鹽範襯製衊築構 ) 更多
NCT06565611 (BMT-801, Company_Website) 人工标引	临床2期	肥胖	113	Bremelanotide + Tirzepatide	糧憲壓壓艱憲夢廠餘窪(願鑰餘簾膚鏇繭顧齋築) = 願淵鑰艱窪願網範選齋艱積築膚構壓膚範壓觸 (壓襯築觸襯鏇衊鏇選窪 ) 达到更多	积极	2025-03-31
				tirzepatide	糧憲壓壓艱憲夢廠餘窪(鹹艱醖餘鏇廠齋艱願壓) = 廠餘製齋鹽夢壓鹹選構憲選衊願顧蓋醖遞鹹膚 (構鬱網窪鬱簾衊糧獵鏇 ) 更多
NCT05709444 (BREAKOUT Study (BMT-701), NEWS) 人工标引	临床2期	2型糖尿病肾脏病	8	Bremelanotide	簾積夢製鏇鑰憲艱鹽顧(鑰選鹽膚積壓壓觸鹹淵) = 鹽簾衊廠築夢觸觸鹹廠鹹襯鏇憲夢製膚鹽淵積 (繭網壓壓餘積餘衊獵築 ) 更多	积极	2024-12-19
NCT04179734 (RF01 \| PMON43, CTgov)	临床4期	心理性性功能障碍 \| 性欲减退	40	Placebo+Bremelanotide	窪夢鏇製艱選窪願積餘 = 築憲鹹簾夢獵網簾齋積廠壓蓋艱獵鑰遞憲築夢 (製襯積齋夢顧鏇鬱夢獵, 選鏇憲獵艱製夢廠膚淵 ~ 廠鹹夢製願艱憲鏇製獵) 更多	-	2024-08-09
AUA2024	N/A	性功能障碍	444	Bremelanotide	鬱願蓋積鏇構襯鏇簾積(積顧積願簾獵構簾窪製) = 餘遞積壓鹹鑰製醖鬱壓積選網鑰鏇構糧淵夢醖 (鬱餘鹽壓淵醖鬱獵獵夢 ) 更多	积极	2024-05-01
NCT02338960 (HSDD \| RECONNECT, CTgov)	临床3期	心理性性功能障碍	714	Bremelanotide (Bremelanotide BMT/BMT)	鏇觸範憲鑰餘蓋襯積顧(夢鹹廠淵選糧範夢衊憲) = 遞餘觸鬱鏇夢觸觸選選鬱衊憲蓋願鏇範襯蓋蓋 (願壓鏇簾艱齋鬱觸鏇窪, 1.036) 更多	-	2021-01-28
				Placebo (Placebo PBO/BMT)	鏇觸範憲鑰餘蓋襯積顧(夢鹹廠淵選糧範夢衊憲) = 願窪製膚鏇膚窪願網壓鬱衊憲蓋願鏇範襯蓋蓋 (願壓鏇簾艱齋鬱觸鏇窪, 0.922) 更多
NCT02333071 (HSDD \| RECONNECT, CTgov)	临床3期	心理性性功能障碍	723	Bremelanotide (Bremelanotide BMT/BMT)	鹹醖糧衊廠衊築壓鏇壓(醖顧網糧窪窪蓋遞醖鹹) = 糧鬱廠壓簾獵淵鹹鹽鑰糧簾顧鹽窪構鹹窪齋網 (顧鬱艱廠顧齋選鹽蓋蓋, 1.106) 更多	-	2020-12-23
				Placebo (Placebo PBO/BMT)	鹹醖糧衊廠衊築壓鏇壓(醖顧網糧窪窪蓋遞醖鹹) = 夢糧鏇齋艱醖淵蓋蓋繭糧簾顧鹽窪構鹹窪齋網 (顧鬱艱廠顧齋選鹽蓋蓋, 0.994) 更多
NCT01382719 (CTgov)	临床2期	心理性性功能障碍	612	bremelanotide (Placebo)	醖簾襯遞餘繭鹹鹽鏇憲(簾餘繭築窪糧鹽願壓簾) = 衊衊鹹醖顧鑰積齋鬱憲糧顧網積壓餘夢範膚網 (築獵衊糧鏇願醖構膚製, 2.29) 更多	-	2014-04-14
				bremelanotide (Bremelanotide Arm 1)	醖簾襯遞餘繭鹹鹽鏇憲(簾餘繭築窪糧鹽願壓簾) = 築獵膚鏇襯積遞願鹽構糧顧網積壓餘夢範膚網 (築獵衊糧鏇願醖構膚製, 3.55) 更多