FSHR agonists(Follicle-stimulating hormone receptor agonists), LHCGR agonists(Luteinizing hormone/Choriogonadotropin receptor agonists), Ovarian follicle stimulants

Therapeutic Areas

NeoplasmsEndocrinology and Metabolic DiseaseUrogenital Diseases

Active Indication

Primary Ovarian InsufficiencyFemale infertility associated with anovulationPolycystic Ovary Syndrome+ [3]

Inactive Indication-

Originator Organization

Ferring BV

Active Organization

Ferring Pharmaceuticals, Inc.Ferring Pharmaceuticals Pty Ltd.

Huiling Pharmaceutical Consulting (Shanghai) Co., Ltd.

Inactive Organization

Ferring Pharmaceuticals A/S

Rechon Life Science AB

License Organization-

Drug Highest PhaseApproved

First Approval Date

United States (27 Aug 1999),

Infertility, Female

Regulation-

Structure/Sequence

Sequence Code 3246α

Sequence Code 3253β

Sequence Code 83626β

105

Clinical Trials associated with Menotropins

ACTRN12624001371583

/ RecruitingPhase 1

A Phase 1, Single Dose Study to Evaluate the Safety and Pharmacokinetics of GB-hMG (Menotropins) for Subcutaneous Injection in Healthy Premenopausal Women

Start Date25 Oct 2024

Sponsor / Collaborator-

CTRI/2024/10/075239

/ Not yet recruitingPhase 4

Comparing treatment efficacy between recombinant FSH LH and recombinant FSH Highly purifiedhuman menopausal gonadotropins(HMG) A Prospective randomized controlled study. - NIL

Start Date15 Oct 2024

Sponsor / Collaborator-

CTRI/2024/09/073446

/ Not yet recruitingNot ApplicableIIT

Comparison of Clomiphene Citrate vs Human Menopausal Gonadotropin for controlled ovarian stimulation in infertile women with decreased ovarian reserve (DOR) - A randomised controlled trial - NIL

Start Date15 Sep 2024

Sponsor / Collaborator-

100 Clinical Results associated with Menotropins

100 Translational Medicine associated with Menotropins

100 Patents (Medical) associated with Menotropins

2,434

Literatures (Medical) associated with Menotropins

01 Mar 2025·JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY

Race and ethnicity, not just insurance, is associated with biologics initiation in asthma and related conditions

Article

Author: Akenroye, Ayobami ; Hvisdas, Christopher ; Louisias, Margee ; Stern, Jessica ; Jackson, John W

BACKGROUND:

There are pre-existing inequities in asthma care.

OBJECTIVES:

We sought to evaluate effect modification by race of the effect of insurance on biologic therapy use in patients with asthma and related diseases.

METHODS:

We conducted inverse probability weighted analyses using electronic health records data from 2011 to 2020 from a large health care system in Boston, Mass. We evaluated the odds of not initiating omalizumab or mepolizumab therapy within 1 year of prescription for an approved indication.

RESULTS:

We identified 1132 individuals who met study criteria. Twenty-seven percent of these patients had public insurance and 12% belonged to a historically marginalized group (HMG). One-quarter of patients did not initiate the prescribed biologic. Among patients with asthma, individuals belonging to HMG had higher exacerbation rates in the period before initiation compared to non-HMG individuals, regardless of insurance type. Among HMG patients with asthma, those with private insurance were less likely to not initiate therapy compared to those with public insurance (odds ratio [OR]: 0.67, and 95% CI: 0.56-0.79). Among non-HMG with asthma, privately insured and publicly insured individuals had similar rates of not initiating the prescribed biologic (OR: 1.02; 95% CI: 0.95-1.09). Among those publicly insured with asthma, HMGs had higher odds of not initiating therapy compared to non-HMGs (OR: 1.16; 95% CI: 1.03-1.31), but privately insured HMG and non-HMG did not differ significantly (OR: 0.99; 95% CI: 0.91-1.07).

CONCLUSIONS:

Publicly insured individuals belonging to HMG are less likely to initiate biologics when prescribed despite having more severe asthma, while there are no inequities by insurance in individuals belonging to other groups.

01 May 2025·F&S science

Chemotherapy-induced diminished murine ovarian reserve model and impact of low-dose chemotherapy on fertility

Article

Author: Donnez, Jacques ; Maurel, Marie-Christine ; Wen, Jen-Yu ; Dolmans, Marie-Madeleine ; Cacciottola, Luciana ; Houeis, Lara ; Dupuy, Laurence ; van der Plancke, Graziella ; Kara, Elodie

OBJECTIVE:

To establish a murine model of chemotherapy-induced diminished ovarian reserve (DOR) and investigate residual fertility after chemotherapy exposure.

DESIGN:

Two different chemotherapy protocols were tested to establish a valid DOR model by comparing follicle densities in mice given either protocol or physiological solution. An ovarian stimulation protocol was then selected from among different gonadotropins by counting the number of day 2 embryos obtained from normal mice. Finally, DOR mice were stimulated 5 and 8 weeks after chemotherapy with the chosen gonadotropin protocols, and day 2 embryos were recovered after mating, as was ovarian tissue for further immunohistologic analyses.

SUBJECTS:

Seventy-two Naval Medical Research Institute mice.

EXPOSURE:

Two different chemotherapy protocols.

MAIN OUTCOME MEASURES:

This study compared day 2 embryo counts in both normal and chemotherapy-induced DOR mice. Ovarian histology and morphology were also investigated by follicle counting and classification, as was immunostaining for apoptosis (cleaved caspase-3), activation (phospho-Akt), and proliferation (Ki67).

RESULTS:

A dose of 12 mg/kg of busulfan (Bu) + 120 mg/kg of cyclophosphamide (Cy) was chosen to establish the DOR model as it significantly reduced the ovarian reserve compared to both control mice (physiological solution) and the 1.2 mg/kg of Bu + 12 mg/kg of Cy protocol, without depleting it completely. When stimulated with 3.75 IU of Menopur, normal mice produced significantly more embryos than DOR mice given 12 mg/kg of Bu + 120 mg/kg of Cy (41.40 ± 14.74 vs. 23.67 ± 15.55 day 2 embryos). Although the follicle count was statistically diminished after single-dose chemotherapy administration, the remaining follicles did not display any difference in terms of apoptosis, activation, or proliferation rates.

CONCLUSION:

We successfully established a chemotherapy-induced DOR model using 12 mg/kg of Bu + 120 mg/kg of Cy, as evidenced by lower, but not completely depleted, follicle numbers and fewer retrieved embryos. Histologic study of ovarian tissue exposed to DOR-inducing chemotherapy revealed that surviving follicles were of the similar quality as tissue not exposed to chemotherapy.

01 Jan 2025·OPHTHALMOLOGY

Longitudinal Changes of Retinal Nerve Fiber Layer and Ganglion Cell–Inner Plexiform Layer in Highly Myopic Glaucoma

Article

Author: Jonas, Jost B ; Lin, Fengbin ; Weinreb, Robert N ; Lam, Dennis S C ; Chen, Meiling ; Sun, Xiaodong ; Xiaokaiti, Dilimulati ; Fang, Zige ; Jiang, Jingwen ; Zhou, Fengqi ; Song, Yunhe ; Jin, Ling ; Kong, Kangjie ; Liu, Xiaoyi ; Zangwill, Linda M ; Li, Fei ; Zhang, Xiulan

PURPOSE:

To describe the longitudinal changes in peripapillary retinal nerve fiber layer (pRNFL) and macular ganglion cell-inner plexiform layer (mGC-IPL) thicknesses in highly myopic eyes with and without glaucoma and to investigate the effects of high myopia (HM) on the sectoral patterns of pRNFL and mGC-IPL thinning.

DESIGN:

Longitudinal cohort study.

PARTICIPANTS:

A total of 243 eyes from 243 individuals with 3-year follow-up were included in this study: 109 eyes in the HM group, 64 eyes in the open-angle glaucoma (OAG) group, and 70 eyes in the highly myopic glaucoma (HMG) group. Based on visual field assessment, 19 OAG eyes and 21 HMG eyes were determined to show progressive disease.

METHODS:

Mean and sectoral pRNFL and mGC-IPL thicknesses were obtained using swept-source OCT. A linear mixed-effects model was used to compare the thinning rates and percentages among groups.

MAIN OUTCOME MEASURES:

Mean and sectoral thinning rates and percentages of pRNFL and mGC-IPL in HM, OAG, and HMG eyes.

RESULTS:

The mean age of the participants was 37.2 ± 11.2 years, and the mean follow-up duration was 3.2 ± 0.3 years. The mean pRNFL thickness changed at rates of -0.44 μm/year, -0.63 μm/year, and -1.17 μm/year in the HM, OAG, and HMG group, respectively (P < 0.001), whereas the mean mGC-IPL thickness changed at rates of -0.10 μm/year, -0.32 μm/year, and -0.41 μm/year in the 3 groups, respectively (P < 0.001). Temporal pRNFL thinning was faster in HMG compared with OAG (-1.24 μm/year vs. -0.45 μm/year; P = 0.002). The mGC-IPL thinning rate in each sector was not significantly different between the HMG and OAG groups (P > 0.05 for all). In contrast to OAG, HMG eyes showed greater percentage thinning rates of pRNFL in the inferior and temporal sectors, with a greater mGC-IPL thinning in the inferonasal sector.

CONCLUSIONS:

The patterns of pRNFL and mGC-IPL thinning differ between HMG and OAG. In particular, faster temporal pRNFL thinning may be a distinguishing feature for identifying glaucoma in HM eyes. These findings also may enhance the understanding of the mechanisms of damage in HMG.

FINANCIAL DISCLOSURE(S):

Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

News (Medical) associated with Menotropins

20 Jun 2024

·www.fiercepharma.com

Ferring launches online assessment tool, educational platform around male fertility

The overall goal of the initiative is to make the entire fertility journey more equitable for both women and men, which, according to Ferring, may ultimately help “improve drop-out rates, decrease stress, address stigma, reduce unnecessary medical costs and accelerate the path to pregnancy.” Ferring Pharmaceuticals is setting the record straight on fertility issues. Because infertility is often branded largely as a women’s issue, many men may be unaware of their own possible role in the matter and may not undergo testing in a timely manner—even though research has shown that men “substantially” contribute to about half of all cases of infertility. The issue is further compounded by stigma that may make men feel emasculated or embarrassed to be struggling with their fertility. A new initiative from Ferring, however, is aiming to boost awareness and education around male fertility and break down that stigma. According to a company announcement Thursday, the program was launched in partnership with Posterity Health, a virtual care service focused on male reproductive health and is hosted on Ferring’s existing Fertility Out Loud platform, which launched in 2021 to provide support for aspiring parents. The platform’s new addition will specifically target men, to “activate them to learn about their fertility health and how it may impact the couple’s path to parenthood,” according to Ali Castro, senior director of marketing and strategic engagement for Ferring’s reproductive medicine division. To do so, it’ll offer both educational resources and a confidential digital assessment that male partners can use to gain a better idea of their personal reproductive health. The overall goal of the initiative is to make the entire fertility journey more equitable for both women and men, which, according to Ferring, may ultimately help “improve drop-out rates, decrease stress, address stigma, reduce unnecessary medical costs and accelerate the path to pregnancy.” “When a couple is having trouble conceiving, the male partner typically waits 22 months before seeking an evaluation—during this period the female is often receiving unnecessary, and in some cases, invasive care,” Pam Pure, co-founder and CEO of Posterity, said in the announcement. “Working together with Ferring, we have made it easier to complete a male fertility assessment from home. Identifying and addressing male factor issues early in the fertility journey will empower couples to take control of their reproductive health.” Both the new initiative and larger Fertility Out Loud platform are unbranded, hosted on a standalone site with the only mention of Ferring at the bottom of each page. That said, Ferring does offer several fertility-related products, including Menopur and Novarel, both of which are used to induce ovulation in women struggling with infertility, and Endometrin, which provides extra progesterone to women who are undergoing fertility treatments.

08 Dec 2023

·synapse.patsnap.com

What are HMG-CoA reductase inhibitors and how do you quickly get the latest development progress?

HMG-CoA reductase is an enzyme that plays a crucial role in the human body's cholesterol synthesis pathway. It is responsible for catalyzing the conversion of HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) to mevalonate, a key precursor in the production of cholesterol. By regulating the activity of HMG-CoA reductase, the body can control the amount of cholesterol synthesized. This enzyme is the target of statin drugs, which inhibit its activity, leading to a reduction in cholesterol levels. Maintaining proper HMG-CoA reductase function is essential for maintaining cholesterol homeostasis and preventing the development of cardiovascular diseases. HMG-CoA reductase inhibitors, also known as statins, are a class of drugs used to lower cholesterol levels in the body. The first statin, lovastatin, was approved by the FDA in 1987. Since then, several other statins have been developed, including atorvastatin, simvastatin, and rosuvastatin. Statins work by inhibiting the enzyme HMG-CoA reductase, which is involved in the production of cholesterol in the liver. By reducing cholesterol levels, statins can help prevent heart attacks, strokes, and other cardiovascular diseases. In addition to their cholesterol-lowering effects, statins have been shown to have other beneficial effects, such as reducing inflammation and improving endothelial function. They have also been investigated for their potential to treat other conditions, such as Alzheimer’s disease, multiple sclerosis, and certain types of cancer. The future of HMG-CoA reductase inhibitors looks promising, with ongoing research into new statins and other cholesterol-lowering drugs. Researchers are also investigating the potential of statins to treat other diseases, such as osteoporosis and autoimmune disorders. However, there are also concerns about the long-term effects of statin use, such as an increased risk of diabetes and liver damage. As such, further research is needed to fully understand the benefits and risks of these drugs. The mechanism of action of HMG-CoA reductase inhibitorsHMG-CoA reductase inhibitors are a class of drugs commonly known as statins. From a biomedical perspective, these drugs are used to lower cholesterol levels in the blood. They work by inhibiting the enzyme HMG-CoA reductase, which plays a crucial role in the production of cholesterol in the liver. By blocking this enzyme, statins reduce the amount of cholesterol synthesized in the body, leading to a decrease in LDL (low-density lipoprotein) cholesterol, often referred to as "bad" cholesterol. Lowering LDL cholesterol levels can help prevent the development of cardiovascular diseases such as heart attacks and strokes. Additionally, statins may have other beneficial effects, such as reducing inflammation and improving the function of blood vessels. HMG-CoA reductase inhibitors are commonly prescribed to individuals with high cholesterol levels or those at risk of cardiovascular diseases. Catalog of HMG-CoA reductase InhibitorsThe currently marketed HMG-CoA reductase inhibitors include: Ezetimibe/Pitavastatin CalciumAtorvastatin/FimasartanFenofibrate/Pitavastatin CalciumAmlodipine Besylate/Fimasartan Potassium Trihydrate/Rosuvastatin CalciumAmlodipine Besylate/Olmesartan Medoxomil/Rosuvastatin CalciumAtorvastatin Calcium Hydrate/Metformin HydrochlorideAtorvastatin/Hydrochlorothiazide/Aspirin/EnalaprilPitavastatin MagnesiumAmlodipine/Losartan Potassium/Rosuvastatin CalciumValsartan/Rosuvastatin CalciumFor more information, please click on the image below. What is the purpose of using HMG-CoA reductase inhibitors?HMG-CoA reductase inhibitors, are used to lower cholesterol levels in the body. They are used adjunctively with diet and exercise to treat and manage hypercholesterolemia (high cholesterol in blood) and for primary and secondary prevention of coronary heart disease. For more information, please click on the image below to log in and search. How can I get the most recent advancements in HMG-CoA reductase inhibitors?In the Synapse database, you can keep abreast of the latest research and development advances of HMG-CoA reductase inhibitors anywhere and anytime, daily or weekly, through the "Set Alert" function. Click on the image below to embark on a brand new journey of drug discovery!

26 Sep 2023

·synapse.patsnap.com

Analysis on the Clinical Research Progress of cholesterol drug

Cholesterol, also known as cholesterin, is a derivative of polycyclic hydrocarbon, widely present in animal bodies, especially abundant in brain and neural tissues. Cholesterol has multiple physiological functions. It not only participates in the formation of cell membranes, but also serves as the raw material for synthesizing bile acids, vitamin D, and steroid hormones. Cholesterol is a waxy substance present in the blood. The body needs cholesterol to build healthy cells, but having too much cholesterol might increase your risk of heart disease. High cholesterol can lead to fatty deposits in your blood vessels. Over time, these deposits grow, limiting the flow of blood through your arteries. These deposits can break suddenly and form a clot that causes a heart attack or stroke. High cholesterol can be genetic but is often preventable and treatable, caused mainly by unhealthy lifestyle habits. A healthy diet, regular exercise, and sometimes medication can help reduce high cholesterol. HMG-CoA Reductase is the rate-limiting enzyme in the biosynthesis of cholesterol in the body, catalyzing the substrate HMG-CoA to produce mevalonic acid. This is the rate-limiting step in the in vivo synthesis of cholesterol. HMG-CoA reductase is an important target of lipid-regulating drugs. Inhibitors of HMG-CoA reductase have similar structural fragments to the substrate HMG-CoA. The affinity of inhibitors for HMG-CoA reductase is greater than that of the substrate. They can inhibit HMG-CoA reductase to produce mevalonic acid, which reduces the synthesis and content of cholesterol in the body, helping to reduce cholesterol, especially low-density lipoprotein cholesterol. Low-density lipoprotein cholesterol is a leading cause of atherosclerosis. Lowering it can slow the progression of atherosclerotic disease, thereby preventing and treating cardiovascular and cerebrovascular diseases. HMG-CoA Reductase Competitive LandscapeAccording to the data provided by Patsnap Synapse-Global Drug Intelligence Database: the following figure shows that as of 25 Sep 2023, there are a total of 139 HMG-CoA reductase drugs worldwide, from 174 organizations, covering 56 indications, and conducting 3252 clinical trials. 👇Please click on the picture link below for free registration or login directly if you have freemium accounts, you can browse the latest research progress on drugs , indications, organizations, clinical trials, clinical results, and drug patents related to this target. The analysis of the target HMG-CoA reductase reveals a competitive landscape with multiple companies making progress in their research and development efforts. Merck & Co., Inc., Hanmi Pharmaceutical Co., Ltd., and Organon & Co. have shown significant growth with multiple approved drugs. The most common indications for drugs targeting HMG-CoA reductase are hyperlipidemias, dyslipidemias, and hypertension. Small molecule drugs dominate the drug type analysis, indicating their effectiveness and widespread use. South Korea, the United States, and the European Union are leading in terms of the number of approved drugs, with China also making progress in this field. Overall, the target HMG-CoA reductase presents a competitive landscape with promising future development potential. The globally approved HMG-CoA reductase inhibitor on the market: SimvastatinSimvastatin is a small molecule drug that belongs to the class of statins. It primarily targets HMG-CoA reductase, an enzyme involved in cholesterol synthesis. This drug has been approved for various therapeutic areas, including Nervous System Diseases, Cardiovascular Diseases, Congenital Disorders, Endocrinology and Metabolic Disease, and Digestive System Disorders. 👇Please click on the image below to directly access the latest data (R&D Status | Core Patent | Clinical Trial | Approval status in Global countries) of this drug. Simvastatin is indicated for the treatment of several conditions, including Heterozygous familial hypercholesterolemia, Hyperlipoproteinemia Type V, Stroke, Hyperlipidemias, Hyperlipoproteinemia Type II, Coronary Disease, Hypercholesterolemia, and Pancreatitis. These indications highlight the drug's effectiveness in managing cholesterol levels and reducing the risk of cardiovascular events. The originator organization of Simvastatin is Merck Sharp & Dohme Corp. This pharmaceutical company played a crucial role in the development and commercialization of the drug. Simvastatin has achieved the highest phase of approval globally. Simvastatin was first approved globally in January 1988. Since then, it has been widely used in clinical practice and has become a cornerstone in the management of hyperlipidemia and related disorders. The drug's long history of use and approval demonstrates its established position in the pharmaceutical market. In summary, Simvastatin is a small molecule drug that targets HMG-CoA reductase and is approved for various therapeutic areas, including Nervous System Diseases, Cardiovascular Diseases, Congenital Disorders, Endocrinology and Metabolic Disease, and Digestive System Disorders. It is indicated for the treatment of conditions such as hyperlipidemia, hypercholesterolemia, and coronary disease. Developed by Merck Sharp & Dohme Corp., Simvastatin has achieved the highest phase of approval globally and in China. Its first approval dates back to January 1988, highlighting its long-standing presence in the pharmaceutical market.

100 Deals associated with Menotropins

External Link

KEGG	Wiki	ATC	Drug Bank
D02692	Menotropins	G03GA02	DB00032

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Primary Ovarian Insufficiency	United States	Ferring Pharmaceuticals, Inc.	19 Feb 2014
Female infertility associated with anovulation	Australia	Ferring Pharmaceuticals Pty Ltd.	13 Sep 2011
Polycystic Ovary Syndrome	Australia	Ferring Pharmaceuticals Pty Ltd.	13 Sep 2011
Anovulation	United States	Ferring Pharmaceuticals, Inc.	29 Oct 2004
Infertility	United States	Ferring Pharmaceuticals, Inc.	29 Oct 2004
Infertility, Female	United States	Ferring Pharmaceuticals, Inc.	27 Aug 1999

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05103228 (CTgov)	Not Applicable	Infertility \| Ovarian Diseases	190	human menopausal gonadotropin+Follitropin delta+Follitropin Alfa (Lower Gonadotropin Dose Stimulation)	frwcdbwzyu = elvcyslunl uppvdupzaw (uhhipjrmat, btcnfisxec - mihnfdirak) View more	-	13 Dec 2024
				human menopausal gonadotropin+Follitropin delta+Follitropin Alfa (Higher Gonadotropin Dose Stimulation)	frwcdbwzyu = wiizrumycz uppvdupzaw (uhhipjrmat, csfsunhweg - vmnrspvfzm) View more
NCT04163458 (CLARA, CTgov)	Phase 3	Infertility	405	Placebo (for MENOPUR powder+MENOPUR solution for injection in pre-filled pen, 1200 IU/1.92 mL (MENOPUR Liquid)	whwngjepom(aurncwcsez) = nyjzhrtrbn klusxsdipe (xxkrogbvfj, 5.5) View more	-	07 Nov 2023
				Placebo (for MENOPUR solution for injection in pre-filled pen)+MENOPUR powder and solvent for solution for injection, 75 IU (MENOPUR Powder)	whwngjepom(aurncwcsez) = lipywnlyzp klusxsdipe (xxkrogbvfj, 4.2) View more
MEGASET-HR (Pubmed \| Pharmacoecon Open)	Not Applicable	-	310	Highly Purified Human Menopausal Gonadotropin (HP-hMG)	rbcpetsqnn(xxgpdouagw) = qbsfrfhcui glmqjtkthq (fvwvicbpfr )	Positive	01 Sep 2023
				Recombinant Follicle Stimulating Hormone (rFSH)	rbcpetsqnn(xxgpdouagw) = gknrvfynxj glmqjtkthq (fvwvicbpfr )
NCT02554279 (MEGASET-HR, Pubmed)	Phase 4	-	620	Highly purified human menotropin (HP-hMG)	egitgxssih(spqcwwbacn) = numsprasnw rfqqigowns (ifvlnuawmb )	-	01 Dec 2020
				Recombinant follicle-stimulating hormone (FSH)	egitgxssih(spqcwwbacn) = jcezxgvagv rfqqigowns (ifvlnuawmb )
NCT02554279 (MEGASET HR, Pubmed \| Fertil Steril) Manual	Phase 4	Ovarian Stimulations	619	highly purified human menotropin	bjxudhfkri(kicwrvmcca) = dipjdxsfdh wvrxowxgsl (kojnjphrms ) View more	Negative	01 Aug 2020
				recombinant follicle-stimulating hormone	bjxudhfkri(kicwrvmcca) = ngzlduampw wvrxowxgsl (kojnjphrms ) View more
SUN-092 (ENDO2020)	Not Applicable	Eunuchism	7	hCG monotherapy	rgslrbhrhu(jotiehdmkt) = zeonksfsuh psyxtrbofi (iwzijonden, 3.18–10.02) View more	Positive	08 May 2020
				hCG+ therapy	rgslrbhrhu(jotiehdmkt) = kfsxsmrcpb psyxtrbofi (iwzijonden, 8.30–11.75) View more
NCT02554279 (MEGASET-HR \| MEGASET HR, CTgov)	Phase 4	Infertility	620	menotropin (Menotropin)	pmtxcmzsxs = jvfbdojnak qkahdxagwo (sluxtafsng, gqmcwmqohw - uznsqcrplu) View more	-	02 Mar 2018
				recombinant FSH (Recombinant FSH)	pmtxcmzsxs = kgeoooxwqn qkahdxagwo (sluxtafsng, gpsxinsjcb - hmtbvhbekp) View more
NCT01921166 (Diminished Ovarian Reserve, CTgov)	Phase 4	Infertility	23	Menopur+Clomid+Bravelle+Follistim+Gonal f (Clomiphene Plus Gonadotropins)	slcpfufhmc = qgqrzefoze bhxpolafyw (ajdxrcafrd, gfnepnhuoe - ulssbxtasi) View more	-	23 Feb 2018
				Leuprolide flare (Leuprolide Flare)	slcpfufhmc = qjmdfcwihc bhxpolafyw (ajdxrcafrd, hvhsqiaiqk - ujcboinkfh) View more
Pubmed \| Gynecol Obstet Fertil Senol	Not Applicable	Ovarian Hyperstimulation Syndrome	421	Highly purified hMG (HP-hMG)	mnvuprezzb(ghsqkyzgfh) = vkewmzzrdi nrwznwrfrg (ysjkheildi, 1.1 - 4.3)	-	01 May 2017
NCT02542280 (CTgov)	Phase 3	Infertility \| Endometritis	360	endometrial injury. (Endometrial Injury)	hnoyucipga = lwukgvswpk pdmvaanfdd (lmawjyonxm, nytrlgezho - fxjipjsfuw) View more	-	08 Jan 2016
				ovarian stimulation (no Endometrial Injury)	hnoyucipga = jqpkglrkgp pdmvaanfdd (lmawjyonxm, oibzmkqexh - zqisamwtnp) View more

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