To verify the non-inferiority of KLH-2109 to leuprorelin acetate in a double-blind manner in terms of efficacy in endometriosis patients with pelvic pain.

开始日期2025-06-09

申办/合作机构

Kissei Pharmaceutical Co., Ltd.

NCT05738382

/ Unknown status临床2期

A Randomized, Double-blind, Open for Active Comparator, Parallel, Multi-center Phase II Study to Explore the Efficacy, Safety and Tolerability of BG2109 Compared With Cetrorelix During COH in Female Subjects Undergoing ART Procedures

To explore the optimal effective daily dose of BG2109 to suppress premature luteinizing hormone (LH) surge during COH in female subjects undergoing ART procedures.

开始日期2023-08-01

申办/合作机构

上海葆正医药科技有限公司

NCT05894135

/ Unknown status临床3期

A Multi-Center, Randomized, Double-Blind, Placebo-Controlled Phase III Study to Evaluate the Efficacy and Safety of BG2109 in Chinese Subjects With Endometriosis

The objective of this study is to demonstrate the efficacy and safety of BG2109 administered orally once daily at a dose of 100 mg alone or of 200 mg in combination with add-back hormone replacement therapy (ABT: estradiol (E2) 1 mg / norethisterone acetate (NETA) 0.5 mg) versus placebo, while under randomized treatment, in the management of moderate to severe endometriosis-associated pain (EAP) in chinese women with surgically confirmed endometriosis

开始日期2023-07-14

申办/合作机构

上海葆正医药科技有限公司

100 项与林扎戈利相关的临床结果

登录后查看更多信息

100 项与林扎戈利相关的转化医学

登录后查看更多信息

100 项与林扎戈利相关的专利（医药）

登录后查看更多信息

项与林扎戈利相关的文献（医药）

2025-10-01·FERTILITY AND STERILITY

Linzagolix with and without hormonal add-back therapy for symptomatic uterine fibroids: PRIMROSE 1 & 2 long-term extension and withdrawal study

Article

作者: Satoshi Hori ; Hugh Taylor ; Francisco Carmona Herrera ; Elke Bestel ; Sven Becker ; Marie-Madeleine Dolmans ; Christian M Becker ; Felice Petraglia ; Jacques Donnez

OBJECTIVE:

To evaluate whether oral linzagolix administered once daily for up to 52 weeks (extension study) at a dose of 100 mg or 200 mg with or without hormonal add-back therapy (ABT) (1.0 mg estradiol; 0.5 mg norethisterone acetate) can maintain the efficacy and tolerability seen at 6 months of therapy and whether there is any recurrence of symptoms (bleeding and pain) after cessation of therapy (withdrawal study).

DESIGN:

PRIMROSE 1 and PRIMROSE 2 were essentially identical, randomized, parallel, double-blind, and placebo-controlled phase 3 trials conducted in women with uterine fibroid-associated heavy menstrual bleeding (HMB) (menstrual blood loss [MBL] of more than 80 mL per cycle over 2 menstrual cycles).

SUBJECTS:

In PRIMROSE 1 and 2, 1,012 women were included in the full analysis set. Eligible subjects were women aged 18 years or older with ultrasound-confirmed fibroids and HMB of at least 80 mL blood loss per cycle for a minimum of two cycles, as determined by the alkaline hematin method. Eligible participants had to have at least one fibroid measuring 2 cm in diameter or more (or multiple small fibroids with overall uterine volume exceeding 200 cm³), but no fibroids greater than 12 cm in diameter.

INTERVENTION:

Eligible women with uterine fibroid-associated HMB were randomly assigned at a 1:1:1:1:1 ratio to one of five masked daily treatment: placebo, 100 mg linzagolix alone, 100 mg linzagolix with hormonal ABT (1 mg estradiol and 0.5 mg norethisterone acetate), 200 mg linzagolix alone , or 200 mg linzagolix with hormonal ABT (1 mg estradiol and 0.5 mg norethisterone acetate). After 24 weeks, patients assigned to the placebo or 200 mg linzagolix alone groups were switched to 200 mg linzagolix with ABT, except in PRIMROSE 1, in which 50% of subjects on a placebo continued with the placebo (random selection) until week 52. All other women continued on the original study medication. Efficacy and safety were evaluated at week 52 (extension study) as well as week 64 (withdrawal study). Bone mineral density was also assessed at week 76 (6 months after cessation of therapy).

MAIN OUTCOME MEASURES:

The primary endpoint was decreased MBL to less than 80 mL and a reduction of more than 50% from baseline. Specifically, this study sought to determine whether the reduction in MBL and other secondary outcomes, such as uterine volume and pain, observed at 24 weeks could be maintained over an extended (52 weeks) treatment period and further withdrawal period.

RESULTS:

In the pooled data from PRIMROSE 1 and PRIMROSE 2 extension studies, the significantly higher proportion of women showing a reduction in HMB in all linzagolix (with or without ABT) treatment groups observed at week 24, was maintained until week 52. Percentages of women with reduced MBL at week 52 (based on the pooled week 52 full analysis set) were 55.0% in the 100 mg group, 86.1% in the 100 mg with ABT group, 76.7% in the 200 mg group/200 mg with ABT, and 89.9% in the 200 mg with ABT group. Of subjects previously treated with linzagolix and in amenorrhea by week 52, 88.8% reported their first bleed or heavy bleeding between weeks 52 and 64. In both PRIMROSE studies, the most common adverse events up to week 52 were hot flushes. Their incidence had returned to baseline values by week 64. Bone mineral density was well preserved in all groups at week 52. In women treated with 200 mg linzagolix alone up to week 24, initial bone mineral density loss (lumbar spine) recovered by week 52 after adding ABT from week 24 onwards.

CONCLUSION:

Findings at 52 weeks confirmed the benefits of treatment observed at 24 weeks. At 52 weeks, linzagolix 100 mg or 200 mg with or without ABT was found to reduce HMB, which is a burden for women with uterine fibroids. Their quality of life was improved. Risks of bone loss and vasomotor symptoms were minimized as a result of ABT administration. Partial suppression with once-daily linzagolix 100 mg without ABT potentially provides a unique option for chronic treatment of symptomatic uterine fibroids in women who do not wish to have ABT or in whom it is contraindicated. The relatively fast recurrence of uterine fibroid-associated symptoms after cessation of therapy is an argument in favor of long-term continuation of treatment.

TRIAL REGISTRATION:

PRIMROSE1 (NCT03070899) PRIMROSE 2 (NCT03070951).

2025-08-01·BJOG-AN INTERNATIONAL JOURNAL OF OBSTETRICS AND GYNAECOLOGY

Pain Reduction in Linzagolix‐Treated Patients With Uterine Fibroids: A Secondary Mediation Analysis of the PRIMROSE 1 and 2 Phase 3 Trials

Article

作者: Boolell, Mitra ; Petraglia, Felice ; Dolmans, Marie‐Madeleine ; Becker, Sven ; Bestel, Elke ; Herrera, Francisco Carmona ; Ionescu‐Ittu, Raluca ; Donnez, Jacques ; Renner, Stefan P. ; St‐Pierre, Julien ; Hori, Satoshi

ABSTRACT:

Objective:

Among women with uterine fibroids (UFs), we assess the extent to which the linzagolix effect on pain alleviation is explained by its effect on reducing heavy menstrual bleeding (HMB) and fibroid volume (FV).

Design:

Post hoc analysis on the pooled data from two randomised double‐blind placebo‐controlled phase 3 trials.

Setting:

94 sites in the US (PRIMROSE 1 trial) and 95 sites in Europe/US (PRIMROSE 2 trial).

Population:

Women aged ≥ 18 years with ultrasound‐confirmed UFs and HMB (n = 1012).

Methods:

Participants were randomised to linzagolix (100 mg and 200 mg, with and without hormonal add‐back therapy) versus placebo. A post hoc mediation analysis was conducted on the pooled PRIMROSE 1 and PRIMROSE 2 data. The effect of linzagolix versus placebo on pain reduction was divided into three components (effect explained by HMB reduction associated with linzagolix, FV reduction associated with linzagolix, and remaining [not yet explained] treatment effect), with proportions of each component reported.

Main Outcome Measures:

The mediation analysis outcome was clinically significant pain reduction, defined as a change of ≥ 2 pain categories from baseline to Week 24 using the Numeric Rating Scale (pain categories: no pain (0), and mild (1–3), moderate (4–6), severe pain (7–10)).

Results:

In the mediation analysis, 28%–51% (depending on treatment arm) of linzagolix effect on pain reduction was explained by its effect on HMB reduction, while 2%–8% was explained by its effect on FV reduction. The residual proportion ranged between 44% and 67%, depending on treatment arm, and was statistically significant only in the linzagolix 200 mg without add‐back therapy arm (p = 0.002).

Conclusions:

This analysis showed that reductions in pain were significantly mediated by reductions in HMB (all doses) and FV (200 mg alone) in linzagolix‐treated women with UFs. Further research is needed to identify additional mediating factors.

Trial Registration:

ClinicalTrials.gov: NCT03070899 and NCT03070951

2025-06-07·Human Reproduction Open

Two-year follow-up study (PRIMROSE 3) to assess bone mineral density in subjects with uterine fibroids completing the PRIMROSE 1 and PRIMROSE 2 linzagolix trials

Article

作者: Taylor, Hugh ; Carmona Herrera, Francisco ; Becker, Sven ; Petraglia, Felice ; Bestel, Elke ; Becker, Christian ; Donnez, Jacques ; Hori, Satoshi ; Dolmans, Marie-Madeleine ; Paszkowski, Maciej

Abstract:

STUDY QUESTION:

How important was the change in lumbar spine (L1–L4), femoral neck, and total hip bone mineral density (BMD) from post-treatment baseline values to 24 months after the end of treatment in PRIMROSE 1 and PRIMROSE 2 study participants?

SUMMARY ANSWER:

In the present study (PRIMROSE 3), mean percentage changes in lumbar spine BMD from the post-treatment baseline to month 24 (primary endpoint) were small in most treatment groups and similar to variations in the placebo group.

WHAT IS KNOWN ALREADY:

Due to its mechanism of action, some BMD decreases are observed with oral GnRH antagonist treatment, depending on the dose administered and addition or not of add-back therapy (ABT) (1 mg oestradiol and 0.5 mg norethisterone acetate). In PRIMROSE 1 and PRIMROSE 2, no significant changes in BMD were observed in any of the three anatomic sites investigated (lumbar spine, femoral neck, and total hip) in any of the treated groups but one. Indeed, at 24 weeks, mean differences were most pronounced in the lumbar spine in participants given 200 mg linzagolix alone.

STUDY DESIGN, SIZE, DURATION:

PRIMROSE 3 is a long-term follow-up study on BMD in subjects who completed at least 20 weeks of treatment in the main linzagolix trials (PRIMROSE 1 or PRIMROSE 2) and underwent dual-energy X-ray absorptiometry (DEXA) within 35 days of their last treatment (week 24 or week 52 [extension study]). The primary endpoint was the change in lumbar spine (L1–L4), femoral neck, and total hip BMD from post-treatment baseline values to 24 months after the end of treatment in PRIMROSE 1 and PRIMROSE 2 study participants. The secondary endpoint was the change in lumbar spine (L1–L4), femoral neck, and total hip BMD from pre-treatment baseline values to 24 months after the end of treatment. The study involved an eligibility visit and up to three follow-up consultations at 12, 18 and/or 24 months after the end of treatment in either PRIMROSE 1 or PRIMROSE 2.

PARTICIPANTS/MATERIALS, SETTING, METHODS:

Patients given an end-of-treatment DEXA scan within 35 days of their last treatment were invited to participate in the PRIMROSE 3 study. Those who were pregnant or unable to undergo a DEXA scan on the same type of equipment as used for the end-of-treatment DEXA scan in PRIMROSE 1 or PRIMROSE 2 were not eligible for this trial. A total of 137 subjects were screened, 134 (97.8%) of whom were enrolled and 130 (94.9%) included in the safety analysis set. Subject groups were small and ranged from 7 subjects (placebo group) to 30 subjects (200 mg/200 mg+ABT group). Most subjects (n = 110, 80.3%) completed the study by evaluation of their BMD by DEXA at 2 years post-treatment.This study (EudraCT number: 2021-000452-19) was conducted at 3 sites in Bulgaria, 4 sites in the Czech Republic, 4 sites in Hungary, 1 site in Latvia, 6 sites in Poland, 1 site in Romania, 5 sites in Ukraine, and 32 sites in the USA.

MAIN RESULTS AND THE ROLE OF CHANCE:

The most notable percentage increase from the end of treatment to month 24 was in the 200 mg/200 mg+ABT treatment group, which was also the group showing the greatest mean percentage BMD loss during linzagolix treatment. This marked upturn in BMD after cessation of treatment demonstrated the crucial role of ABT.Percentage changes in lumbar spine BMD from the pre-treatment baseline to month 24 (secondary endpoint) remained above −2% in all linzagolix treatment groups. Small BMD modifications observed from both the post-treatment and pre-treatment baseline to month 24 after the end of therapy may not have any clinically relevant impact on overall bone health of linzagolix-treated individuals, since the Z-score of most subjects was within the expected range for age. In addition, changes in BMD values and Z-scores in the linzagolix treatment groups were mostly within the same range as in the placebo group.

LIMITATIONS, REASONS FOR CAUTION:

The number of patients is relatively small. Since interpretation of results from the month-12 and month-18 visits is limited due to the small number of subjects in each treatment arm at corresponding time points, giving rise to high data variability, this manuscript focuses on the month-24 visit only.

WIDER IMPLICATIONS OF THE FINDINGS:

It can be assumed that the small BMD changes observed from both the post-treatment and pre-treatment baseline to month 24 after cessation of therapy may not have any clinically relevant impact on overall bone health of linzagolix-treated individuals.Changes in BMD values and Z-scores in the linzagolix treatment groups were mostly within the same range as in the placebo group, indicating that there are no long-term consequences on BMD after the end of linzagolix treatment.

STUDY FUNDING/COMPETING INTEREST(S):

Funding for the PRIMROSE studies was provided by ObsEva (Geneva, Switzerland). Analysis of data was partially supported by ObsEva (Geneva, Switzerland), Theramex (London, UK), and Kissei (Japan). Grant 5/4/150/5 was awarded to M.-M.D. by the FNRS.J.D. was a member of the scientific advisory board of ObsEva and Preglem until 2023 and reports consulting fees from ObsEva, Gedeon Richter, and Theramex. F.P. has received consulting fees and honoraria for lectures from Theramex. H.T. has received grants from Abbvie, reports consulting fees from ObsEva and Gedeon Richter, has a patent on endometriosis biomarkers owned by Yale University, and was a past president of American Society of Reproductive Medicine (ASRM). C.B. was a member of the independent data monitoring board for the PRIMROSE trials and member of the advisory board for Spirit 1 and 2 trials. He was also the Chair for the ESHRE endometriosis guideline committee. Consulting fees from Myovant and Theramex went to the University of Oxford. S.B. has received consulting fees and honoraria for lectures from Theramex. F.C.H. reports consulting fees and honoraria for lectures, presentations, or educational events from Theramex and Gedeon Richter and receiving honoraria for participation in a data safety monitoring board for Organon. M.P. was a principal investigator in the ObsEva-sponsored PRIMROSE 2 and 3 trials. E.B. and S.H. are employees of Theramex. M.-M.D. has received fees for lectures from Gedeon Richter and Theramex.

TRIAL REGISTRATION NUMBER:

EudraCT number: 2021-000452-19.

项与林扎戈利相关的新闻（医药）

2026-04-12

·環球通海外醫藥

这19种救命药，日本早就能买到了，中国患者还在等

去年冬天，我接触到一个小细胞肺癌患者的家属。化疗两轮，耐药了。医生说国内能用的方案基本走完了，让他们"做好心理准备"。家属不甘心，到处找。最后发现一个叫塔拉妥单抗的新药——美国批了，日本也批了，临床数据漂亮得吓人：40%的缓解率，中位生存期14个月。但中国没有。他问我，能不能从日本买到。那时候我第一次认真研究了日本PMDA的审批清单，越查越沉默。不是一两个药的问题，而是整整一批——19个近年获批的重磅处方药，日本患者已经在用了，中国要么还在临床，要么连申报都没开始。后来那个患者等到了好消息。今年4月11号，塔拉妥单抗正式获得中国NMPA批准。但更多的人，还在等。这篇文章，就把这份清单摊开给你们看。先看全貌 19个药，两张命运不同的处方我把2023到2026年日本PMDA获批的重点处方药做了个表。每一行背后都是一群真实的患者。 📋 表格说明中国未上市审评/临床中已获批 Leniolisib Joenja ｜罕见免疫缺陷 APDS 🇯🇵 2026.3 🇨🇳 连申报都没交 Palovarotene Sohonos ｜"人体石化症" FOP 🇯🇵 2026.2 🇨🇳 还在准备资料 Garadacimab Andembry ｜遗传性血管水肿 HAE 🇯🇵 2025.2 🇨🇳 审评中 / 优先审评 Sebetralstat Ekterly ｜遗传性血管水肿急救 🇯🇵 2025.12 🇨🇳 没影 Sepiapterin Sephience ｜苯丙酮尿症 PKU 🇯🇵 2025.12 🇨🇳 没影 Avacincaptad pegol Izervay ｜黄斑变性地理萎缩 🇯🇵 2025.9 🇨🇳 还在二期临床 Odevixibat Bylvay ｜婴幼儿胆汁淤积肝病 🇯🇵 2025.9 🇨🇳 桥接研究中 Bempedoic acid Nexletol ｜高胆固醇降脂 🇯🇵 2025.9 🇨🇳 准备申报 Palopegteriparatide Yorvipath ｜甲状旁腺功能减退 🇯🇵 2025.8 🇨🇳 没批 Vornorexant Vorzzz ｜失眠 🇯🇵 2025.8 🇨🇳 二期临床 Sepetaprost Setaneo ｜青光眼 🇯🇵 2025.8 🇨🇳 没影 Atogepant Aquipta ｜偏头痛预防 🇯🇵 2026.2 🇨🇳 在审评 Linzagolix Yselty ｜子宫肌瘤 🇯🇵 2025.12 🇨🇳 三期临床 Aceneuramic acid Acenobel ｜GNE肌病 🇯🇵 2024.3 🇨🇳 急需申报阶段 Apadamtase alfa Adzynma ｜先天性TTP 🇯🇵 2024.3 🇨🇳 没批 Acoramidis Beyonttra ｜心脏淀粉样变 🇯🇵 2025.3 🇨🇳 准备申报 Concizumab Alhemo ｜血友病 🇯🇵 2023.9 🇨🇳 快了，在审 Sotatercept Airwin ｜肺动脉高压 🇯🇵 2025.6 🇨🇳 2026.1 已获批 ✅ Tarlatamab Imdelltra ｜小细胞肺癌 🇯🇵 2025.10 🇨🇳 2026.4 已获批 ✅ 最后两个画了绿勾的，是好消息——中国赶上来了。剩下的17个，还在等。有的等一年，有的等三年，有的不知道要等多久。那些等不起的人 STORY 01 "人体石化症"：全身肌肉慢慢变成骨头先说个你可能从没听过的病——FOP，进行性骨化性纤维发育不良。中国大概有六七百个患者。他们的肌肉、肌腱、韧带会一点一点变成骨头。不是比喻，是真的长出骨头。每一次碰撞、跌倒，甚至一次感冒引发的炎症，都可能触发一轮新的骨化。而且不可逆——长出来的骨头永远不会消失。很多患者到了二三十岁就完全不能动了。最残酷的是，你连手术都做不了。切掉异位骨？身体会在手术创口长出更多的骨头。 💊 Palovarotene（Sohonos） 🇯🇵 日本获批：2026年2月 📊 新发骨化病灶减少：54% 🇨🇳 中国：临床前资料准备阶段不能治愈，但能让"石化"的速度慢下来。对这些患者来说，每减少一块异位骨，就多保住一分活动能力。六七百个人的事，你说少不少？放到14亿人里可以忽略不计。但对每一个家庭来说，那就是百分之百。 STORY 02 一辈子不能吃肉的孩子苯丙酮尿症（PKU），这个病知道的人多一些了。新生儿筛查里经常查的一项。中国大概有十万以上的患者。他们的身体无法正常代谢苯丙氨酸，一旦摄入过多蛋白质，苯丙氨酸就会在血液里堆积，损伤大脑。所以PKU患者从出生起就不能吃正常食物。不能吃肉、不能吃鸡蛋、不能吃豆腐、不能喝牛奶。主食只能吃特制的低蛋白米面——很贵，口感很差。一辈子。之前有个药叫沙丙蝶呤，但只对一部分患者有效，大概四分之一到一半的人能用。 💊 Sepiapterin（Sephience） 🇯🇵 日本获批：2025年12月 📊 血苯丙氨酸水平降低：51.9% 📊 达到安全水平的比例：63.8% ⭐ 关键突破：对沙丙蝶呤无效的患者也管用 🇨🇳 中国：无公开注册进度更关键的是，用了这个药之后，患者可以增加天然蛋白质的摄入。翻译成人话就是：这些孩子可能终于可以吃一口正常的饭了。中国？无公开注册进度。 STORY 03 等不到明天的眼睛地理萎缩，这个名字听起来像地理课，其实是眼科的事。它是晚期干性黄斑变性的表现。视网膜上的感光细胞一块一块地死掉，视野中央出现一个黑洞，而且这个黑洞会越来越大。看不清人脸。看不清药瓶上的字。看不清路。最后什么都看不清。全球大概五百万人有这个问题。中国老龄化加速，患者数量在快速增长。之前全世界没有任何一个获批的药物能治这个。"GA无药可治"是眼科教科书上的标准答案。 💊 Avacincaptad pegol（Izervay） 🇯🇵 日本获批：2025年9月 📊 视力退化速度减慢：35%—40% 💉 给药：每月一次眼内注射 🇨🇳 中国：还在二期临床，获批预计1—2年不能逆转，不能治愈，但能让患者多"看见"几年。对一个七十多岁的老人来说，一到两年意味着什么，不用我说。不只是罕见病的事你可能觉得，上面说的都是罕见病，跟普通人没关系。那说几个你身边可能就有的。 😴 失眠 · 3亿人现有安眠药要么容易上瘾，要么第二天昏昏沉沉。日本去年8月批了 Vorzzz（就是这个名字，来自打呼噜的"Zzz"），新一代机制，起效快，半衰期短，第二天不影响正常工作。 🇨🇳 中国还在二期临床 🤯 偏头痛 · 1.5亿人现有的预防药都要打针。日本今年2月批了 Aquipta（atogepant），口服的，每天一粒，不用打针。 🇨🇳 中国在审评了，但还没批 ❤️🩹 高胆固醇 · 上亿人他汀是主力药，但大概10%—15%的人吃他汀肌肉疼得受不了。日本去年批了 Nexletol，这个药只在肝脏里激活，不走肌肉那条路，完美避开肌肉副作用。 🇨🇳 中国还在准备注册申报 🩺 子宫肌瘤 · 育龄女性25%—30% 月经量大到贫血，很多人最后不得不切子宫。日本去年底批了 Yselty（linzagolix），口服的，能大幅减少出血量，可能帮很多人保住子宫。 🇨🇳 中国还在三期临床这些不是什么天价孤儿药。它们面对的是数以千万计甚至上亿的患者群体。好消息：有些差距正在缩小也不全是坏消息。今年最让人振奋的两件事： ✅ 好消息一 Sotatercept（治肺动脉高压）。日本2025年6月批的，中国NMPA用了快速审评通道，2026年1月就批了。前后不到七个月。 ✅ 好消息二开头说的塔拉妥单抗。日本2025年10月批，中国2026年4月批。半年。这说明NMPA的审评改革是实实在在起了作用的。"第3号公告"推动下，一些重磅品种的审批速度已经追上来了。但这两个是明星品种——一个治癌症，一个治致命性心血管病，社会关注度高，企业推动力强。更多的药，尤其是罕见病领域的，没有那么大的舆论推力，也没有那么大的商业回报去驱动快速审评。它们只能慢慢排队。等不及的人怎么办说到这里，可能有人要问了：既然中国没批，那这些药就完全买不到吗？不是。跨境购药是一个合法存在的通道。简单说就是通过正规的境外持牌药房采购，以个人自用的名义进口。但这条路的门槛不低：你得找到靠谱的渠道，确认药品是正品，处理冷链物流（很多生物制剂需要2-8度保存），还要有专业的用药指导。自己搞，基本搞不定。现在市面上有一些专业的跨境医药服务平台在做这件事。我了解到的几个关键判断标准： 1 看牌照有没有正规的药品经营资质？比如香港卫生署的药品批发牌照，这是目前最被认可的跨境医药合规资质之一。 2 看供应链有没有自己的海外仓？药品从哪里采购？物流用的什么链路？生物制剂的冷链能不能保障？ 3 看服务有没有药师审核处方？有没有用药指导？出了问题有没有售后？ 4 看价格正规渠道的价格一般比美国便宜很多（日本药价通常是美国的十分之一），但比自己飞去日本买贵一些——多出来的部分是物流、合规和服务成本。这些大家可以自己做功课判断。写在最后整理这份清单的时候，我反复想到一句话： "世界上最远的距离不是生与死而是药已经被发明出来了你却用不上。" 这不是药企的错——全球同步上市是不现实的，每个国家都有自己的审评流程和监管逻辑。这也不是NMPA的错——他们确实在改革，速度确实在加快。但对于正在等待的患者和家属来说，政策的改善是以年为单位的，而疾病的进展是以天为单位的。如果这篇文章里的某个药名，恰好是你或你家人正在寻找的—— 去查，去问，去想办法。不要只是等。当然，最重要的一句话还是要说：任何药物都要在专业医生指导下使用。跨境购药解决的是"有没有"的问题，但"该不该用、怎么用"这个问题，只有你的主治医生能回答。 📚 信息来源日本PMDA官网（pmda.go.jp）、中国NMPA药品审评中心（cde.org.cn）、各药企公开披露资料、ClinicalTrials.gov。药品审批状态持续变化，文中信息截至2026年4月，如有更新以各国药监局最新公示为准。 ⚠️ 本文不构成医疗建议。觉得有用？转发给需要的人长按关注「环球通医药」不错过每一个新药资讯

申请上市临床3期优先审批临床结果临床2期

2026-03-26

·拜尔迪生物

【AmBeed揭秘】月经不调、长痘长胖？当心“多囊”找上门！一文带你全面解码PCOS

姐妹们，你是否也有这样的困扰：月经总是“随心所欲”，脸上痘痘“此起彼伏”，体重秤上的数字还悄悄上涨？如果你中了不止一条，那可要当心了。这可能不只是简单的内分泌失调，而是“多囊卵巢综合征”（PCOS）在悄悄作祟。今天，我们用一篇硬核干货，带你彻底看懂PCOS。 01. 什么是多囊卵巢综合征(PCOS)? PCOS 是一种高度异质性的家族性疾病，病因尚未完全明确，目前认为与遗传、表观遗传、发育及环境因素密切相关。过去，诊断多聚焦于生殖特征（如月经不调、高雄激素、卵巢多囊样改变）。但近年研究证实，它更是一种代谢性疾病：约60%的正常体重患者和94%的肥胖患者存在胰岛素抵抗，且这些代谢异常还会遗传给直系亲属，包括男性亲属的代谢紊乱风险增加[1] 简单来说，PCOS 是一个涉及生殖、内分泌和代谢的复杂综合征。根据国际广泛采纳的诊断标准，满足以下三项中的两项，并排除其他可能引起类似症状的疾病后，即可诊断为PCOS[2]：高雄激素血症/表现:体内雄激素过高，表现为长痘（痤疮）、体毛增多（多毛）、脱发等。排卵功能障碍:表现为月经稀发（周期>35天）、闭经（超过3-6个月不来月经）或不孕。卵巢多囊样改变:通过B超检查，发现卵巢里有很多长不大的“小卵泡”（单侧≥20个），像一串串未成熟的小葡萄，但没有优势卵泡发育和排出。 ⚠️ 请注意：仅有B超显示“多囊样改变” 并不等于就是PCOS！很多正常女性也可能有此表现，必须结合临床症状和激素水平综合诊断。 02. PCOS的四副"面孔":你是哪一型？ PCOS 的困扰千人千面,每个人的表现都不尽相同。2025年发表于Nature Medicine的一项涉及上万名患者的研究，将 PCOS 精准划分为四种主要亚型[3]： 1. 高雄激素型 (Hyperandrogenic PCOS) ：核心特征：雄激素水平显著升高,是“痘痘肌”和“小胡子”的重灾区。健康风险：代谢紊乱问题较突出，血脂异常风险高，孕期可能面临更高的流产风险。 2. 肥胖型 (Obesity PCOS) ：核心特征：以高 BMI，肥胖为主要表现，胰岛素抵抗非常明显。健康风险：是四种亚型中代谢问题最严重的一种，糖尿病、高血压和脂肪肝风险最高，IVF助孕的成功率也相对较低。 3. 高性激素结合球蛋白型 (High-SHBG PCOS) ：核心特征：体内一种叫做“性激素结合球蛋白”（SHBG）的蛋白质水平较高，它能“捆绑”住雄激素，使其活性降低。健康风险：这是最“温和”的类型，代谢风险最低，生殖结局也相对最好。 4. 高LH-AMH型 (High LH-AMH) ：核心特征：黄体生成素（LH）和抗缪勒管激素（AMH）水平双高，主要表现为生殖问题。健康风险：代谢问题不突出，但卵巢储备功能“过于旺盛”，在进行IVF促排卵时，发生“卵巢过度刺激综合征”的风险最高。 03. 硬核揭秘：身体里到底发生了什么？ PCOS 的病理机制核心是高雄激素、胰岛素抵抗和下丘脑 - 垂体 - 卵巢（HPG）轴紊乱的相互作用，三者形成恶性循环，且涉及组织功能异常、分子信号通路紊乱等多重层面。 1. 高雄激素：疾病进展的 "核心推手" 图1 PCOS雄激素合成相关信号通路 [4] 60%-75% 的 PCOS 患者存在高雄激素血症，过高的雄激素会阻碍卵泡成熟，导致排卵障碍和卵巢多囊样改变；同时还会促进脂肪细胞肥大、抑制脂肪生成，加剧胰岛素抵抗，且能通过表观遗传方式影响代际传递，增加后代患病风险。 PCOS患者卵泡膜细胞中CYP17A1表达上调，导致雄激素积累过多，内源性类固醇生成失调。同时，在卵巢颗粒细胞中，也有一种可将雄激素转化为雌激素的酶——CYP19A1，在PCOS中被发现表达下调，从而抑制了雄激素向雌激素的转化[5]。 LH-cAMP/PKA 通路：PCOS 患者下丘脑 - 垂体 - 卵巢轴紊乱，LH 分泌升高，与卵泡膜细胞表面的 LHR（LH 受体）结合。LHR 激活后启动腺苷酸环化酶（AC），使细胞内 cAMP 水平升高，进而激活蛋白激酶 A（PKA）。PKA 进入细胞核后，通过磷酸化 CREB 等转录因子，直接促进卵泡膜细胞中 CYP17A1 的表达，增强雄激素合成；同时，PCOS 患者颗粒细胞中 AKAP95 水平降低，导致 PKA 锚定细胞核能力下降，CREB 磷酸化减弱，间接抑制 CYP19A1 表达，减少雄激素向雌激素转化[6]。 IRS-PI3K-AKT 通路：胰岛素与卵泡膜细胞表面胰岛素受体结合，激活受体后磷酸化胰岛素受体底物（IRS-1/2）。磷酸化的 IRS-1/2 激活磷脂酰肌醇 3 - 激酶（PI3K），PI3K 将 PIP2 转化为 PIP3，进而激活 AKT。AKT 一方面直接增强 CYP17A1 的活性，另一方面与 cAMP/PKA 通路协同，放大雄激素合成效应；同时，该通路在颗粒细胞中表达降低，导致下游 PDK1、mTOR 等分子表达减少，影响颗粒细胞功能，间接加剧激素失衡[7]。 NF-κB 炎症通路：卵泡液中 TNF-α、S100-A9 等炎症因子激活卵泡膜细胞和颗粒细胞中的 NF-κB 通路。激活的 NF-κB 进入细胞核后，一方面促进卵泡膜细胞中 CYP17A1 的表达，增强雄激素合成；另一方面在 mRNA 和蛋白水平显著抑制颗粒细胞中 CYP19A1 的表达，阻断雄激素转化，形成 “炎症→激素失衡→炎症加重” 的恶性循环[8]。 Wnt 通路：Wnt 通路激活后，通过胞内信号分子（如 β-catenin）调控转录因子活性，间接增强卵泡膜细胞中CYP17A1的表达，从而促进孕烯醇酮、孕酮向脱氢表雄酮（DHEA）、雄烯二酮（A）等雄激素转化[9]。 2. 胰岛素抵抗 (IR)：幕后“大黑手” 图2 PCOS中的胰岛素抵抗 [10] 核心起始异常：胰岛素受体及 IRS-1 的丝氨酸过度磷酸化PCOS患者中，胰岛素受体及 IRS-1 的丝氨酸（Serine）位点发生过度磷酸化，这种异常磷酸化阻碍了 IRS 的酪氨酸（Tyrosine）位点正常磷酸化（pY），导致 IRS 无法有效激活下游信号通路[11]。信号传导链中断：PI3K/Akt 通路抑制PI3K/Akt 通路抑制：IRS 功能异常直接导致 PI3K 激活不足，PIP2 向 PIP3 的转化受阻，进而使 PDK1 和 Akt/PKB 无法被有效激活，信号传导链中断[12]。代谢功能障碍：葡萄糖摄取与糖原合成双受损[13]葡萄糖摄取障碍：Akt/PKB 未被激活，无法驱动 GLUT-4 向细胞膜转移，导致细胞表面 GLUT-4 表达减少，葡萄糖无法有效进入细胞，加速血糖升高。糖原合成受抑：Akt/PKB 对 GSK3 的抑制作用消失，GSK3 持续处于活性状态，抑制 GS 的功能，导致肝脏、肌肉等组织的糖原合成减少，无法有效储存葡萄糖，进一步加重糖代谢紊乱。次级异常放大：MAPK 通路异常激活与连锁反应[14]MAPK 通路异常激活：异常磷酸化同时激活 MAPK 通路，进一步放大胰岛素抵抗效应，且可能间接促进雄激素合成酶的激活，加剧 PCOS 的高雄激素血症。代偿性高胰岛素血症及危害：代偿性高胰岛素血症是胰腺为克服外周胰岛素抵抗而过量分泌胰岛素所致，其核心危害是加剧高雄激素相关异常：直接刺激卵巢卵泡膜细胞增生，增强 LH 受体与类固醇合成酶活性以促进雄激素分泌；抑制肝脏合成 SHBG，升高游离雄激素水平，加重多毛、痤疮；上调 IGF-1 活性，协同 LH 进一步刺激雄激素生成，最终形成 “胰岛素抵抗 - 高雄激素” 恶性循环。 3. 神经内分泌调节异常 HPG 轴的神经内分泌调节异常是 PCOS 生殖功能障碍的核心，涉及 GnRH 脉冲生成、垂体激素分泌、卵巢反馈调节等多个层面的紊乱：图3 神经内分泌轴失调 [15] GnRH 脉冲频率异常：下丘脑 GnRH 脉冲发生器对雌激素、孕激素的负反馈敏感性下降（由高雄激素介导），导致 GnRH 脉冲频率和幅度增加。这种异常脉冲会优先刺激垂体分泌 LH（黄体生成素），而促卵泡生成素（FSH）分泌相对不足，形成 LH/FSH 比值升高的典型特征（常见于 LH-PCOS 亚型）[16]。垂体 - 卵巢信号失衡的直接影响：过高的 LH 会持续刺激卵巢卵泡膜细胞合成雄激素，而 FSH 不足会导致卵泡发育停滞在小窦卵泡阶段，无法形成优势卵泡，最终引发排卵障碍和卵巢多囊样改变；同时，卵巢小窦卵泡数量增多会分泌过量抗穆勒氏管激素（AMH），AMH 会进一步增强 GnRH 神经元活性，放大 GnRH 脉冲异常，加重 HPG 轴紊乱，形成 "神经内分泌 - 卵巢功能" 恶性循环[17]。分子调控机制：KNDy 神经元（表达 kisspeptin、神经激肽 B、强啡肽 A）是 GnRH 脉冲的关键调控者，PCOS 患者 KNDy 神经元功能异常，导致 kisspeptin 分泌紊乱，进而影响 GnRH 释放；此外，高胰岛素血症会直接刺激下丘脑 GnRH 基因表达，增强垂体 LH 分泌，进一步加剧 HPG 轴失衡[15]。 4.脂肪组织功能障碍：代谢与炎症的桥梁图4 PCOS中的脂肪功能障碍 [15] 形态与功能异常：脂肪分布异常：中心性肥胖为主，内脏脂肪比例升高，脂肪细胞肥大（较 BMI 匹配对照组大 30%-50%），且与高雄激素水平正相关。脂代谢紊乱：脂解作用增强，游离脂肪酸（FFA）释放增加，导致肝脏、胰腺等非脂肪组织脂毒性沉积。脂肪因子失衡：抗炎因子（脂联素）降低 30%-50%，促炎因子（瘦素、抵抗素）升高 2-4 倍，进一步抑制胰岛素信号。关键酶异常：皮下脂肪组织中醛酮还原酶 1C3（AKR1C3）表达升高，催化雄烯二酮转化为睾酮，局部雄激素活化加剧胰岛素抵抗，且胰岛素可上调 AKR1C3 活性，形成恶性循环[15]。 04 治疗方法：从对症管理到精准干预目前 PCOS 治疗以改善症状、预防并发症为目标，结合亚型特征实现个体化干预[18]： 1.生活方式干预：所有亚型的基础治疗！体重管理：即使仅减轻5%的体重，也能显著改善胰岛素抵抗和生殖功能，肥胖型患者需重点控制 BMI。饮食与运动：低糖、高纤维饮食结合规律运动，可改善血糖血脂代谢，降低炎症水平。 2.药物治疗：针对性缓解核心症状胰岛素增敏剂：如二甲双胍，可改善胰岛素抵抗，恢复排卵，适用于代谢异常明显的患者。抗雄激素药物：如螺内酯、环丙孕酮，能缓解多毛、痤疮等高雄激素症状，需注意避孕。调节月经周期：口服避孕药可规律月经、降低高雄激素，适用于无生育需求者；孕激素可周期性调节月经。促排卵治疗：克罗米芬、来曲唑等用于有生育需求的患者，不同亚型需调整用药方案，避免卵巢过度刺激 📚 参考文献 1.Nat Rev Endocrinol. 2025 Apr;21(4):230-244.2.Human Reproduction, 2023, 38(9), 1655–16793.Nat Med. 2025 Dec;31(12):4214-4224.4.生殖医学杂志2022年1月第31卷第1期5.Endocr Rev. 2016 Oct;37(5):467-520.6.Am J Physiol Endocrinol Metab. 2013 Sep 15;305(6):E736-44.7.Signal Transduct Target Ther. 2022;7(1):216.8.Hum Reprod. 2012;27(12):3560-3568.9.Theranostics. 2024 May 27;14(8):3385-3403.10.Stem Cell Rev Rep. 2023 May;19(4):853-865.11.Hum Reprod. 2007 Apr;22(4):1003-10.12.J Ethnopharmacol. 2020 Mar 25;250:111965.13.Signal Transduct Target Ther. 2022;7(1):216.14.Endocr Rev. 2012 Dec;33(6):981-1030.15.Nat Rev Endocrinol. 2025 Apr;21(4):230-244.16.Nat Rev Dis Primers. 2024 Apr 18;10(1):27.17.Nat Rev Endocrinol. 2021 Sep;17(9):521-533.18.Nat Rev Endocrinol. 2018 May;14(5):270-284. 高雄激素型（HA-PCOS） Spironolactone (A243260) 靶点/作用机制：Androgen Receptor Spironolactone是一种醛固酮受体拮抗剂，IC50为 7.1 nM，通过竞争性阻断肾远曲小管盐皮质激素受体，减少K⁺排泄/H⁺分泌。 Cyproterone acetate (A264009) 靶点/作用机制：Androgen Receptor Cyproterone acetate是抗雄激素受体的拮抗剂和部分激动剂，IC50 为 7.1 nM，EC50 为 4 μM。 Atorvastatin Calcium Salt Trihydrate (A563943) 靶点/作用机制：HMGCR Atorvastatin Calcium Salt Trihydrate是一种广泛使用的降胆固醇药物，主要通过抑制HMG-CoA还原酶来降低血清胆固醇水平。它用于治疗高胆固醇血症和相关心血管疾病。 Flutamide (A208282) 靶点/作用机制：Androgen Receptor Flutamide是一种非甾体类雄激素受体（AR）拮抗剂，通过竞争性结合雄激素受体，阻断睾酮和二氢睾酮（DHT）的作用，从而抑制前列腺癌细胞的生长。其活性代谢物2-羟基氟他胺具有更高的AR亲和力，常用于研究前列腺癌，特别是在与GnRH类似物联合使用时效果显著。 Finasteride (A201116) 靶点/作用机制：5α-还原酶 Finasteride是一种强效、可逆的 II 型 5α-还原酶抑制剂，对 II 型酶的 IC50 为 4.2 nM，Ki 为 10.2 nM，主要用于研究良性前列腺增生 (BPH) 和男性型脱发 (MPB)。 Estradiol (A805521) 靶点/作用机制：ERR Estradiol是一种雌激素激素，是内源性雌激素受体（ER）主要配体，激活ERα/β调控生殖系统发育，通过非基因组作用激活PI3K-Akt/mTOR通路促进细胞增殖，并负反馈抑制下丘脑GnRH释放。用于更年期综合征及低雌激素血症。肥胖型（OB-PCOS） Semaglutide (A753934) 靶点/作用机制：GLP-1 Semaglutide 是一种长效人类 GLP-1 类似物，作为 GLP-1 受体激动剂，常用于 2 型糖尿病的研究。 Orlistat (A512085) 靶点/作用机制：Lipase Orlistat 是一种可逆性脂肪酶抑制剂（IC50 = 122 ng/mL），可用于肥胖、动脉粥样硬化及细胞增殖的研究。 Metformin (A270611) Metformin (1,1-Dimethylbiguanide) 通过抑制肝脏中的线粒体呼吸链来激活 AMPK，增强胰岛素敏感性，可用于 2 型糖尿病研究。Metformin 能透过血脑屏障，诱导自噬 (autophagy)。 Liraglutide (A608103) 靶点/作用机制：GLP-1 Liraglutide是一种胰高血糖素样肽-1（GLP-1）受体激动剂，常用于2型糖尿病的临床治疗。 Benazepril (A651804) 靶点/作用机制：ACE Benazepril 是一种血管紧张素转换酶（ACE）抑制剂，常用于高血压、心力衰竭及慢性肾病相关机制研究。 Fenofibrate (A763996) 靶点/作用机制：PPARα Fenofibrate 是一种 PPARα 激动剂（EC50 = 30 μM），并可抑制 CYP2C19（IC50 = 0.2 μM）和 CYP2B6（IC50= 0.7 μM），适用于脂质代谢及胆固醇调控机制研究。 High-SHBG PCOS Norethisterone (A542979) 靶点/作用机制：Progesterone Receptor Norethisterone是一种合成孕激素，模拟内源性卵巢激素的作用，常用于研究子宫内膜异位症和由激素水平异常引起的子宫出血及继发性闭经。 (-)-Norgestrel (A422801) 靶点/作用机制：Progesterone Receptor (-)-Norgestrel是一种合成孕激素，作为一些激素避孕药的活性成分，作用于孕酮受体。 Drospirenone (A689592) 靶点/作用机制：Progesterone Receptor Drospirenone是一种合成孕激素，属于螺内酯的类似物，主要用于激素替代疗法及相关研究。 Dydrogesterone (A178769) 靶点/作用机制：Progesterone Receptor Dydrogesterone是一种强效、口服活性的孕激素，适用于多种与孕激素缺乏相关的妇科疾病。高LH-AMH型（High LH-AMH PCOS） Linzagolix (A1544041) 靶点/作用机制：GNRH Receptor Linzagolix（KLH-2109; OBE-2109）是一种有效的、非肽类、口服活性的GnRH拮抗剂，用于子宫肌瘤、子宫内膜异位症和子宫腺肌症的研究。 Ganirelix acetate (A1146548) 靶点/作用机制：GNRH Receptor Ganirelix acetate是一种注射用促性腺激素释放激素 (GnRH) 拮抗剂，通过竞争性抑制GnRH受体，迅速降低雌二醇水平。该化合物可用于卵巢过度刺激综合征（OHSS）的研究，常用于生殖医学中以控制排卵。 Relugolix (A261708) 靶点/作用机制：GNRH Receptor Relugolix是一种口服活性的 GnRH 拮抗剂，IC50 值分别为 0.33 nM（人）和 0.32 nM（猴），用于性激素依赖性疾病研究。 Elagolix sodium (A136268) 靶点/作用机制：GNRH Receptor Elagolix sodium是一种人类 GnRH 受体（GnRHR）拮抗剂，IC50 和 Ki 值分别为 0.25 nM 和 3.7 nM，具有口服活性，广泛用于促性腺激素释放激素受体研究。北京拜尔迪生物是AmBeed的授权代理商，更多产品，欢迎咨询订购！北京拜尔迪热线：010-62960866 网址：www.biodee.net 北京拜尔迪生物(BioDee)，成立于2003年，国家级高新技术企业，多个进口品牌和优秀国产品牌的一级代理商，专注于生命科学领域，为客户提供试剂、耗材、仪器等产品，涵盖了细胞生物学、微生物学、植物学、分子生物学、生物化学、免疫学等领域。

2026-03-24

·allsci.com

Insilico partners with ASKA Pharma on AI-driven target discovery for gynecological diseases

Insilico Medicine and ASKA Pharmaceutical have entered a research collaboration to identify novel therapeutic targets for gynecological conditions including endometriosis, uterine fibroids, and adenomyosis. Cambridge, Massachusetts-based Insilico Medicine (HKEX: 3696), a clinical-stage company using generative AI for drug discovery, will deploy its PandaOmics target identification engine to generate and prioritize candidate targets. Tokyo-based ASKA Pharmaceutical, which focuses on internal medicine, obstetrics, and gynecology, will validate the AI-predicted targets for translational potential. The deal expands an existing relationship in which ASKA has been a user of Insilico’s AI software. Financial terms of the collaboration were not disclosed. The press release does not specify upfront payments, milestone structures, royalties, or equity components. The absence of disclosed economics is consistent with early-stage research collaborations where the primary deliverable is target nomination rather than compound development or clinical advancement. The collaboration operates at the earliest stage of drug discovery: target identification and validation. No specific drug candidate has been named. Insilico will use PandaOmics, its AI-driven biological data analysis platform, which integrates multi-modal omics data and biomedical text mining to generate disease hypotheses and rank candidate targets. The company recently introduced TargetPro, a framework within PandaOmics that builds disease-specific models to predict which targets are most likely to advance into clinical development. ASKA will then apply its gynecological disease expertise to experimentally validate the computationally nominated targets. The three indications covered by the deal represent areas with limited mechanistic diversity in approved therapies. Endometriosis affects approximately 190 million women globally according to World Health Organization estimates. Uterine fibroids and adenomyosis affect larger populations and frequently co-occur. Current pharmacological options include GnRH-based therapies, particularly in endometriosis and uterine fibroids, including AbbVie’s elagolix (Orilissa) and the Myovant Sciences/Pfizer relugolix combination (Myfembree). There is no US FDA-approved drug specifically indicated for adenomyosis; management typically relies on off-label hormonal therapy, symptom control, procedures, or surgery depending on severity and fertility goals. • Elagolix (Orilissa) — AbbVie — marketed for endometriosis pain; AbbVie’s elagolix-containing combination product Oriahnn is marketed for heavy menstrual bleeding associated with uterine fibroids. • Relugolix combination (Myfembree) — Myovant/Pfizer — marketed for endometriosis and uterine fibroids • Linzagolix (Yselty) — Gedeon Richter — marketed in the EU for uterine fibroids and symptomatic endometriosis Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

上市批准

100 项与林扎戈利相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D11609	-	-	-

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
子宫肌瘤	日本	Kissei Pharmaceutical Co., Ltd.	2025-12-22
子宫内膜异位症	欧盟	Theramex Ireland Ltd.	2024-12-20
子宫内膜异位症	冰岛	Theramex Ireland Ltd.	2024-12-20
子宫内膜异位症	列支敦士登	Theramex Ireland Ltd.	2024-12-20
子宫内膜异位症	挪威	Theramex Ireland Ltd.	2024-12-20
平滑肌瘤	欧盟	Theramex Ireland Ltd.	2022-06-14
平滑肌瘤	冰岛	Theramex Ireland Ltd.	2022-06-14
平滑肌瘤	列支敦士登	Theramex Ireland Ltd.	2022-06-14
平滑肌瘤	挪威	Theramex Ireland Ltd.	2022-06-14

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
疼痛	临床3期	日本	Kissei Pharmaceutical Co., Ltd.	2022-10-11
Primrose 综合征	临床3期	-	-	2021-08-30
月经过多	临床3期	美国	ObsEva SA	2017-04-20
卵巢过度刺激综合征	临床2期	中国	上海葆正医药科技有限公司	2023-08-01
Cohen综合征	临床2期	中国	上海葆正医药科技有限公司	2022-09-27
Cohen综合征	临床2期	中国	Kissei Pharmaceutical Co., Ltd.	2022-09-27
女性不孕症	临床2期	中国	Kissei Pharmaceutical Co., Ltd.	2022-09-27
女性不孕症	临床2期	中国	上海葆正医药科技有限公司	2022-09-27
子宫腺肌病	临床2期	法国	ObsEva SA	2018-04-23
肝损伤	临床1期	美国	ObsEva SA	2019-05-15

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


NCT03070951 \| NCT03070899 (PRIMROSE 2, Pubmed \| Fertil Steril)	临床3期	子宫肌瘤	1,012	Linzagolix 100 mg	範顧膚顧蓋醖憲簾積觸(鹽鬱積鑰網齋廠夢蓋願) = hot flushes 淵齋觸積餘廠獵衊簾鬱 (願憲窪夢鑰鑰積夢鑰繭 ) 更多	积极	2025-10-01
				Linzagolix 100 mg with ABT
NCT04372121 (EDELWEISS 5, CTgov)	临床3期	子宫内膜异位症	30	LGX (LGX 75 mg)	膚積簾憲廠鏇壓餘鑰網(壓淵鏇夢糧鏇鏇築願積) = 襯憲憲齋顧艱壓窪觸築顧鹹壓選淵簾膚膚築夢 (壓膚憲構積積築範積膚, 0.0) 更多	-	2025-03-19
				LGX (LGX 200 mg+ABT)	膚積簾憲廠鏇壓餘鑰網(壓淵鏇夢糧鏇鏇築願積) = 構窪鏇鹽繭襯範蓋廠鹽顧鹹壓選淵簾膚膚築夢 (壓膚憲構積積築範積膚, 0.0) 更多
NCT03986944 (CTgov)	临床3期	子宫内膜异位症	85	Placebo capsule to match Add-back capsule	顧夢窪襯齋顧選鑰獵簾(構築衊餘廠膚鑰鬱醖餘) = 齋憲遞選鏇顧築鏇遞鏇襯鹹壓壓膚網鹹衊顧鏇 (蓋鏇顧蓋繭襯艱夢醖鹽, 0.5) 更多	-	2024-10-29
NCT05445167 (KLH2302, NEWS)	-	子宫肌瘤	89	Linzagolix	築衊膚遞鑰積醖齋衊範(鏇餘襯衊鑰壓壓淵艱願) = Clinical results have reached the endpoint 選糧憲鬱艱蓋遞網簾顧 (糧衊願糧鑰獵艱範襯鬱 )	积极	2024-07-16
				安慰剂
NCT03992846 (EDELWEISS 3, CTgov)	临床3期	子宫内膜异位症	486	Placebo capsule to match Add-back capsule	鹽繭繭鏇廠顧淵觸壓網 = 觸網選壓遞艱遞簾製艱窪夢簾簾壓衊獵醖製獵 (蓋夢憲獵膚繭構廠蓋淵, 衊夢繭願衊鑰艱廠鏇範 ~ 網壓醖構醖構鬱憲範遞) 更多	-	2024-05-29
NCT04335591 (CTgov)	临床3期	子宫内膜异位症	356	LGX (LGX 75 mg)	範膚遞築簾遞築顧鑰蓋 = 夢膚窪選齋襯鬱網鑰蓋鏇構壓醖鹽壓窪獵醖願 (夢製鏇窪壓遞網鏇鹹齋, 構淵艱積窪醖壓憲蓋鑰 ~ 構築淵獵網網窪鏇艱獵) 更多	-	2024-04-30
				LGX (LGX 200 mg+ABT)	範膚遞築簾遞築顧鑰蓋 = 觸蓋顧獵鹽願夢鑰顧願鏇構壓醖鹽壓窪獵醖願 (夢製鏇窪壓遞網鏇鹹齋, 願築選鏇醖窪網鏇壓壓 ~ 壓夢鬱遞艱獵顧製衊蓋) 更多
NCT03992846 (EDELWEISS 3, Pubmed)	临床3期	子宫内膜异位症 \| 疼痛一线	486	Placebo	鹹選願簾繭鹹簾醖築齋(餘獵廠壓遞鑰觸餘艱願) = 鬱齋繭齋糧蓋糧壓構顧網淵構艱窪鏇繭蓋顧製 (壓簾顧鹹觸選廠遞範築 )	积极	2024-04-22
				Linzagolix 75 mg	鹹選願簾繭鹹簾醖築齋(餘獵廠壓遞鑰觸餘艱願) = 獵範鹹願網襯簾鬱糧獵網淵構艱窪鏇繭蓋顧製 (壓簾顧鹹觸選廠遞範築 )
NCT03070951 (PRIMROSE 2, GlobeNewswire) 人工标引	临床3期	子宫肌瘤	535	add-back therapy+linzagolix	繭糧衊網糧構鏇簾顧淵(壓鏇糧鬱築構遞憲膚廠) = 願繭齋繭蓋鏇鬱壓範淵築繭廠夢壓衊窪簾願廠 (網艱選鬱壓糧夢積鹹網 )	积极	2020-07-06
				linzagolix	繭糧衊網糧構鏇簾顧淵(壓鏇糧鬱築構遞憲膚廠) = 膚廠蓋範醖憲顧鹽鑰淵築繭廠夢壓衊窪簾願廠 (網艱選鬱壓糧夢積鹹網 )