Project title: Comparing the Efficacy of Different Elonva (Corifollitropin Alfa) Protocols in Poor Responders undergoing IVF cycles: Follicular Phase Start vs. Luteal Phase Start, and the Double dose Elonva

Start Date23 Aug 2025

Sponsor / Collaborator

Avicenna Research Institute

NCT06193135

/ RecruitingNot ApplicableIIT

Usefulness of Corifollitropin α as Alternative to Conventional Daily rFSH Protocols in Oocyte Donors Undergoing Pituitary Suppression With Medroxiprogesterona Acetate (MPA)

IVF patients frequently experience physical, emotional or physicological burden; this is particularly relevant in the case of oocyte donors, since young women undergo a procedure that is of no health benefit to them. One of the phases of the treatment that contributes most to this situation is ovarian stimulation; as it involves the administration of daily injections which, in addition to the discomfort of administration, causes anxiety to the patient about its correct administration and possible side effects and to physicians concerns about patient compliance.
Advances in pharmacology and knowledge of ovarian pathophysiology have led to the development of new protocols that simplify and reduce drug administration, decrease the potential risk of misapplication and contribute to an improved patient experience. In this context, Corifollitropin α, a long-acting recombinant FSH (rFSH) molecule, provides with a single subcutaneous injection similar results as daily administration of rFSH during a week.
On the other hand, conventional stimulation protocols used in ART resort to using a GnRH analogue (agonist or antagonist) to prevent early luteinization, which is defined as the presence of a progesterone value of > 1.5 ng/ml on the day of induced ovulation. Nevertheless, its use presents some disadvantages, such as it being sometimes complex to achieve desensitization or consistent hypothalamic block, risk of OHS when ovulation is triggered with HCG or its cost. Hence the interest in exploring new options to prevent a premature peak in LH. Nowadays, the oral administration of progestagens (progesterone-primed ovarian stimulation [PPOS]) during the follicular phase of ovarian stimulation (OS) has emerged as an attractive alternative to conventional protocols for preventing early luteinization. Moreover, PPOS produces a similar or even better, in some subgroups, response to OS (length of treatment, number of MII, cancelation rate, etc.), reproductive outcomes (pregnancy rate, live birth rate, etc) and safety (rate of ovarian hyperstimulation [OHSS] or congenital malformations).
Thus, PPOS would seem to be an effective option for personalized protocols, particularly when fresh embryo transfer (FET) is not to be performed, a circumstance that is likely to rise in frequency given the progressive increase in women's age at childbearing; for example, in oocyte donation, or in fertility preservation (FP) and preimplantation genetic testing for aneuploidy (PGT-A). However, very little data are available regarding cycle outcome following Corifollitropin α and PPOS as pituitary suppressor.
The present study, a prospective RCT, was designed to evaluate cycle characteristics (MII oocytes as the primary objective) and endocrinologic profiles of oocyte donors receiving Corifollitropin α and MPA as co-treatment compared with those receiving a daily dose of rFSH (follitropin β) as a control.

Start Date08 Jul 2025

Sponsor / Collaborator

Instituto Valenciano de Infertilidad SL

NCT06175832

/ RecruitingPhase 4IIT

PPOS and CFA for Elective Freeze-all Ovarian Stimulation Cycles: a Prospective Cross-over Study

P-CCROSS is a randomized, prospective monocentric phase 4 study with a crossover study design. The aim of the study is to compare patient satisfaction (by means of questionnaires) and treatment compliance with IVF treatment with CFA (corifollitropin alfa) and PPOS (Progestin-Primed Ovarian Stimulation) versus conventional IVF treatment with a recombinant FSH/GnRH antagonist. The study will also compare patients undergoing elective fertility preservation versus PGT-A (pre-implantation genetic testing for aneuploidy) patients.The study will have a crossover design so that patients will receive both forms of treatment. The investigators will also compare the endocrine profile and ovarian response of CFA/PPOS versus rFSH/GnRH ovarian stimulation cycles.

Start Date27 Jan 2025

Sponsor / Collaborator

Ghent University Hospital

[+1]

100 Clinical Results associated with Corifollitropin alfa

100 Translational Medicine associated with Corifollitropin alfa

100 Patents (Medical) associated with Corifollitropin alfa

1,394

Literatures (Medical) associated with Corifollitropin alfa

01 Apr 2026·JOURNAL OF ETHNOPHARMACOLOGY

Protective role of alkaloids of Calanthe fimbriata against ethanol-induced gastric ulcer in mice: Involvement of anti-gastric acid secretion and suppression of NF-κB/MAPK inflammatory cascades

Article

Author: Zhang, Hailong ; Chen, Liya ; Wang, Ruyue ; Yu, Chunping ; Yang, Minfei ; Wang, Zhigang ; Gao, Yang ; Zhang, Changlong

ETHNOPHARMACOLOGICAL RELEVANCE:

Calanthe fimbriata is a Tujia ethnomedicine, with a history of use in the therapy of gastric ulcer, chronic hepatitis, etc. Previous investigations indicated its potent protective efficacy against ethanol-induced gastric injury, with alkaloids potentially being the main active constituents.

AIM OF THE STUDY:

This study aimed to validate the protective role of the alkaloids of C. fimbriata (CfA) in ethanol-induced gastric ulceration and to elucidate their mechanisms of action.

MATERIALS AND METHODS:

The gastroprotective efficacy of CfA was evaluated in an ethanol-induced gastric ulcer mouse model. Mechanisms were investigated via ELISA kits, RT-qPCR, and Western blotting. Chemical constituents were isolated and identified through various chromatographic and spectroscopic techniques. Molecular docking was employed to predict the potential targets of active compounds.

RESULTS:

CfA considerably ameliorated stomach mucosal damage induced by ethanol, as indicated by a reduced ulcer area, decreased submucosal edema, improved glandular architecture, and diminished loss of epithelial cells. CfA inhibited gastric acid secretion via up-regulation of PGE₂ and down-regulation of gastrin and H⁺K⁺-ATPase. Moreover, CfA enhanced antioxidant ability by increasing SOD activity and lowering MDA content in both serum and gastric tissue. It also helped maintain NO levels, thereby preserving gastric mucosal integrity. Furthermore, CfA markedly alleviated inflammation by restraining the MAPK and NF-κB cascades, which consequently decreased the generation of pro-inflammatory cytokines. A phytochemical investigation identified two new indole alkaloids, as well as eight known alkaloids from CfA. Molecular docking studies revealed that the two new indole alkaloids exhibited potent binding affinities with PTGER4, p38 MAPK, and NF-κB p65, suggesting their potential as key bioactive components responsible for the mucosa-repairing and anti-inflammatory activities of CfA.

CONCLUSION:

CfA protects against ethanol-induced gastric ulcers in mice through anti-gastric acid secretion, antioxidant, and inhibition of NF-κB/MAPK inflammatory cascades. The two newly identified indole alkaloids are proposed as promising active constituents contributing to these protective effects.

06 Mar 2026·Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology

[Study on the role of annexin A5 in temporomandibular joint osteoarthritis in rats].

Article

Author: Liang, F ; Wang, H ; Zhang, L M ; Liu, J ; Lyu, X X ; Liu, C K ; Huang, S

Objective: To systematically explore the intervention efficacy of annexin A5(AnxA5 on temporomandibular joint osteoarthritis (TMJOA) induced by complete Frend's adjuvant (CFA) in rats. Methods: Thirty-two 6-week-old male SD rats (weighing 200-250 g) were assigned to histological analysis (n=20) or micro-CT analysis (n=12). The TMJOA model was established by bilateral intra-articular injection of CFA, while the control group received saline. Three days later, TMJOA rats were randomly divided into three groups (n=8 each): CFA model group (saline injection), CFA+HA group [hyaluronic acid (HA), once weekly for 2 weeks], and CFA+AnxA5 group (AnxA5 injection every 3 days for 4 injections). The saline group was injected with the same frequency and dosage of saline as that of AnxA5. The changes in the structure of the temporomandibular joint were observed through HE and safranin O-eosin green staining, and the total thickness of the cartilage (TC), the thickness of the hypertrophic chondrocyte layer (HL), the thickness of the fibrocartilage layer (FL), as well as the thickness of the anterior band (A), Intermediate zone (In) and posterior bands (P) of the articular disc were measured.The changes in the content of glycosaminoglycans in the condylar cartilage matrix were observed by Alcian blue and toluidine blue staining. The contents of MMP 13, collagen Ⅱ and TNF-α in the condylar cartilage matrix were observed by Immunohistochemical staining. The infiltration quantity of M1-type macrophages was observed by immunofluorescence staining. The situation of subchondral bone remodeling of the condyle was observed by micro-CT, data such as bone volume fraction (BV/TV), trabecular number (Tb.N), and trabecular thickness (Tb.Th) were collected and calculated. Results: The results of HE and safinin-O fast green staining showed that compared with the thickness of each layer of cartilage and the thickness of the articular disc in the saline group [TC: (306.85±39.87) μm, HL: (123.16±27.19) μm, FL: (43.87±7.01) μm, A: (263.55±13.55) μm, In: (155.91±26.80) μm, P: (263.12±36.21) μm], the TC and HL in the CFA model group were significantly thinner [(218.30±38.32) and (79.90±18.54) μm ](P<0.001), FL was significantly thicker [(67.69±13.46) μm] (P<0.001), and the A, In and P of the articular disc were significantly thicker [respectively (305.27±23.37), (200.96±18.75) and (321.92±16.86) μm] (P<0.001)Compared with the CFA model group, the TC [(252.76±32.23) and (270.37±21.87) μm] and HL [(108.15±11.13) and (108.41±17.30) μm] in the CFA+HA treatment group and the CFA+AnxA5 intervention group were significantly thicker (P<0.05), while FL [(46.08±5.99) and (45.58±5.27) μm] was significantly thinner (P<0.01). The thickness of the A, In and P of the articular disc in the CFA+HA treatment group [(272.54±19.66), (180.24±14.47) and (273.79±29.28) μm] and in the CFA+AnxA5 intervention group [(263.66±10.68), (168.60±9.87) and (279.31±25.79) μm] were significantly thinner (P<0.05). The results of Alcian blue and toluidine blue staining showed that in the saline group, the staining of the condylar hypertrophic layer was obvious and uniform, while in the CFA model group, it was lightly stained, and in some areas, it was even unstained. After treatment with HA and AnxA5, the staining became relatively intense, and the loss of glycosaminoglycans slowed down.The IHC staining results showed that compared with the saline group (MMP13: 0.24±0.03,COL-Ⅱ:0.36±0.12), the content of MMP13 increased (0.37±0.07), and the content of COL-Ⅱ decreased (0.16±0.03) (both P<0.001). Compared with the CFA model group, the CFA+HA treatment group and the CFA+AnxA5 intervention group showed significantly decreased MMP13 levels (0.29±0.04 and 0.29±0.08) (both P<0.05) and significantly increased COL-Ⅱ levels (0.21±0.04 and 0.22±0.03, both P<0.01).The results of HE and IF staining showed that compared with the saline group, there was a large infiltration of inflammatory cells in the synovium of rats in the CFA model group and the number of M1-type macrophages increased (P<0.001). Compared with the CFA model group, both the CFA+HA treatment group and the CFA+AnxA5 intervention group showed a significant reduction in M1 macrophage numbers (P<0.05, P<0.01). The IHC staining results showed that compared with the saline group, the content of TNF-α in the CFA model group increased (P<0.001), while in the CFA+HA treatment group and CFA+AnxA5 intervention group, the content of TNF-α decreased (P<0.05;P<0.001).The Micro-CT results showed that compared with the saline group, the CFA model group exhibited significant decreases in condylar BV/TV, Tb.N, and Tb.Th (P<0.001, P<0.01, P<0.001).The difference between the CFA+HA treatment group and the CFA model group was not statistically significant. Compared with the CFA model group, the CFA+AnxA5 intervention group showed significantly higher BV/TV, Tb.N and Tb.Th (P<0.01, P<0.05, P<0.05). Conclusions: In the CFA-induced inflammation-dominated rat TMJOA model, AnxA5 can protect cartilage homeostasis, inhibit synovial inflammatory response, and simultaneously improve abnormal subchondral bone remodeling.

01 Mar 2026·MICROBIAL PATHOGENESIS

Regulatory role of quercetin, cinnamaldehyde, and glycerol monolaurate complex on lipid metabolism and antiviral mechanisms against white spot syndrome virus in Penaeus vannamei

Article

Author: Li, Yaobing ; Xie, Songhui ; Zhang, Tengwen ; Pan, Luqing ; Yu, Xin ; Chen, Zhengxu

This study investigated the distinct regulatory effects of a novel complex feed additive (quercetin: cinnamaldehyde: glycerol monolaurate = 1:1:2) on lipid metabolism, immune response, and antiviral defense in Penaeus vannamei (initial weight of 0.40 ± 0.13 g). During a 42-day feeding trial, both 0.1 % and 0.2 % complex feed additive (CFA)-supplemented groups modulated hepatopancreatic lipid metabolism by co-regulating the constitutive co-activator of PPARγ (CCPG) and the PI3K-AKT and PTGS2 pathways, promoting lipolysis, suppressing lipid synthesis, and significantly reducing lipid accumulation in the body and plasma (P < 0.05). CFA also activated the JAK-STAT pathway and specifically modulated the NF-κB and p38 MAPK-AP-1 pathways, significantly improving the hemocyte count (THC) and phagocytic activity (PA), and upregulating the expression of antimicrobial peptides and lysozyme, while suppressing inflammatory factors (TNFα, IL16) in both hemocytes and the intestine (P < 0.05). Moreover, CFA improved gut microbiota composition, with key differential genera positively correlating with host immune indices. Under white spot syndrome virus (WSSV) challenge, CFA significantly inhibited viral replication and infection (P < 0.05), thereby enhancing antiviral efficacy and improving shrimp survival, with the best results observed at the 0.2 % concentration. Collectively, this study demonstrates that dietary supplementation with 0.2 % CFA effectively regulates lipid metabolism and strengthens both innate and antiviral immunity in P. vannamei, providing mechanistic insights into host-pathogen interactions and the development of antibiotic alternatives for sustainable aquaculture.

News (Medical) associated with Corifollitropin alfa

02 Jul 2024

·www.prnewswire.com

INOVIO Announces Appointment of Steven Egge as Chief Commercial Officer

Mr. Egge brings over 25 years of biopharmaceutical experience building commercial organizations and successfully launching novel therapeutic products INOVIO poised to become a commercial-stage company with plans to submit a Biologics License Application for INO-3107 in second half of 2024 under U.S. Food and Drug Administration's Accelerated Approval Pathway PLYMOUTH MEETING, Pa., July 2, 2024 /PRNewswire/ -- INOVIO (NASDAQ:INO), a biotechnology company focused on developing and commercializing DNA medicines to help treat and protect people from HPV-related diseases, cancer, and infectious diseases, today announced the appointment of Steven Egge as Chief Commercial Officer. Mr. Egge will lead the company's commercial strategy and operations as it prepares to potentially launch its first DNA medicine product, INO-3107 as a treatment for recurrent respiratory papillomatosis (RRP). "We are delighted to welcome Steve to INOVIO and look forward to adding his expertise to our leadership team as we continue advancing our preparations to commercially launch INO-3107 in 2025, should it receive approval by the FDA as a treatment for RRP," said Dr. Jacqueline Shea, INOVIO's President and Chief Executive Officer. "Steve joins us at an exciting time, as we prepare to become a commercial-stage company, while advancing multiple product candidates targeting unmet medical needs. His expertise launching new products, driving market share in competitive environments, and growing overall therapeutic areas will be advantageous to the development and implementation of our commercial plans, as will his experience across immunology and vaccines, HPV, and rare diseases." "This is a great time to join INOVIO as the company has the opportunity to market the first therapeutic option for patients suffering from RRP, a rare and debilitating HPV-related disease that significantly impacts quality of life," said Mr. Egge. "I look forward to working with the talented team at INOVIO and continuing the ongoing efforts to build out the company's commercial strategies and capabilities." Mr. Egge comes to INOVIO from Sumitomo Pharma (formerly Myovant Sciences, acquired by Sumitovant Biopharma, a subsidiary of Sumitomo Pharma, in 2023), where as Senior Vice President and General Manager for Women's Health he was responsible for building the commercial leadership team, accelerating the launch of Myfembree® and helping lead the company's expansion into new indications. Mr. Egge was at Merck for twenty years, where he held a number of senior commercial leadership roles, including leading Merck's HPV Vaccines Franchise as well as Chief Marketing Officer for the Vaccine Division, where he oversaw launches for new indications for GARDASIL®, a re-launch of ZOSTAVAX®, and launch planning for GARDASIL9® and VAXELIS®. Mr. Egge also served as Global Commercial Head for Merck's Fertility Franchise, where he oversaw the launch of ELONVA® in ex-U.S. markets. After Merck, Mr. Egge served as Senior Vice President at Genfit Corp., a French biotech company focused on liver diseases, where he led commercial planning and business development. About INOVIO's DNA Medicines Platform INOVIO's DNA medicines platform has two innovative components: precisely designed DNA plasmids, delivered by INOVIO's proprietary investigational medical device, CELLECTRA®. INOVIO uses proprietary technology to design its DNA plasmids, which are small circular DNA molecules that work like software the body's cells can download to produce specific proteins to target and fight disease. INOVIO's proprietary CELLECTRA® delivery devices are designed to optimally deliver its DNA medicines to the body's cells without requiring chemical adjuvants or lipid nanoparticles and without the risk of the anti-vector response historically seen with viral vector platforms. About INOVIO INOVIO is a biotechnology company focused on developing and commercializing DNA medicines to help treat and protect people from HPV-related diseases, cancer, and infectious diseases. INOVIO's technology optimizes the design and delivery of innovative DNA medicines that teach the body to manufacture its own disease-fighting tools. For more information, visit . CELLECTRA® is a trademark of INOVIO. GARDASIL®, GARDASIL9®, ZOSTAVAX® and ELONVA® are trademarks of Merck and Co., Inc. VAXELIS® is trademark of The MSP Vaccine Company. Myfembree® is trademark of Sumitomo Pharma Switzerland GmbH. Forward-Looking Statements This press release contains certain forward-looking statements relating to our business, including our plans to develop and commercialize DNA medicines and expectations regarding our research and development programs, including the planned submission of a BLA in the second half of 2024 and the planned commercial launch of INO-3107 if regulatory approval is obtained. Actual events or results may differ from the expectations set forth herein as a result of a number of factors, including uncertainties inherent in pre-clinical studies, clinical trials, product development programs and commercialization activities and outcomes, the availability of funding to support continuing research and studies in an effort to prove safety and efficacy of electroporation technology as a delivery mechanism or develop viable DNA medicines, our ability to support our pipeline of DNA medicine products, the ability of our collaborators to attain development and commercial milestones for products we license and product sales that will enable us to receive future payments and royalties, the adequacy of our capital resources, the availability or potential availability of alternative therapies or treatments for the conditions targeted by us or collaborators, including alternatives that may be more efficacious or cost effective than any therapy or treatment that we and our collaborators hope to develop, issues involving product liability, issues involving patents and whether they or licenses to them will provide us with meaningful protection from others using the covered technologies, whether such proprietary rights are enforceable or defensible or infringe or allegedly infringe on rights of others or can withstand claims of invalidity and whether we can finance or devote other significant resources that may be necessary to prosecute, protect or defend them, the level of corporate expenditures, assessments of our technology by potential corporate or other partners or collaborators, capital market conditions, the impact of government healthcare proposals and other factors set forth in our Annual Report on Form 10-K for the year ended December 31, 2023, our Quarterly Report on Form 10-Q for the quarter ended March 31, 2024, and other filings we make from time to time with the Securities and Exchange Commission. There can be no assurance that any product candidate in our pipeline will be successfully developed, manufactured, or commercialized, that the results of clinical trials will be supportive of regulatory approvals required to market products, or that any of the forward-looking information provided herein will be proven accurate. Forward-looking statements speak only as of the date of this release, and we undertake no obligation to update or revise these statements, except as may be required by law. Contacts Media: Jennie Willson (267) 429-8567 [email protected] Investors: Thomas Hong (267) 440-4298 [email protected] SOURCE INOVIO Pharmaceuticals, Inc.

Executive ChangeVaccine

100 Deals associated with Corifollitropin alfa

External Link

KEGG	Wiki	ATC	Drug Bank
D08895	Corifollitropin alfa	G03GA09	DB09066

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Hypogonadism	European Union	Organon NV	25 Jan 2010
Hypogonadism	Iceland	Organon NV	25 Jan 2010
Hypogonadism	Liechtenstein	Organon NV	25 Jan 2010
Hypogonadism	Norway	Organon NV	25 Jan 2010
Infertility, Female	European Union	Organon NV	25 Jan 2010
Infertility, Female	Iceland	Organon NV	25 Jan 2010
Infertility, Female	Liechtenstein	Organon NV	25 Jan 2010
Infertility, Female	Norway	Organon NV	25 Jan 2010

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Polycystic Ovary Syndrome	Phase 3	Belgium	Merck Sharp & Dohme Corp.	01 Nov 2017
Azoospermia	Phase 3	-	Organon & Co.	11 Feb 2013
Hemochromatosis	Phase 3	-	Organon & Co.	11 Feb 2013
secondary testicular failure	Phase 3	-	Organon & Co.	11 Feb 2013
Infertility	Phase 3	-	Organon & Co.	26 Sep 2006
Ovarian Stimulations	Phase 3	-	Organon & Co.	27 Jun 2006
Complications associated with artificial fertilization	Phase 2	-	Organon & Co.	19 May 2003
Female infertility associated with anovulation	Phase 2	-	Organon & Co.	01 Aug 2001

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05815719 (Alicante protocol, CTgov)	Phase 4	-	30	Corifollitropin Alfa (Study Group)	saauhnhmov(pezlspjuxn) = sgrdiiqgjp qanyzplnfq (pycfcuweon, 6.904) View more	-	18 May 2025
				Human follicle stimulating hormone+Follitropin Alfa (Control Group)	saauhnhmov(pezlspjuxn) = ilmhlngwig qanyzplnfq (pycfcuweon, 6.105) View more
NCT03019575 (MK-8962-043 \| 8962-043, CTgov)	Phase 3	secondary testicular failure \| Hemochromatosis	17	hCG+Corifollitropin alfa	jzuorfsfvx(mwylsvyiqx) = idppmwaqgs soowpxruvw (ushtcgkyfm, 0.7) View more	-	08 Apr 2021
NCT03816670 (Pubmed \| J Assist Reprod Genet)	Not Applicable	Ovarian Stimulations	113	CFα late-start	edecblqkws(gdixlgtthw) = sghhelfzhh uvdmdnfxap (jndeveqgxw ) View more	-	01 May 2020
				CFα standard start	edecblqkws(gdixlgtthw) = tcerbmeyuo uvdmdnfxap (jndeveqgxw )
NCT03816670 (Pubmed 1 \| Pubmed 2 \| J Assist Reprod Genet)	Phase 4	Ovarian Stimulations	113	Corifollitropin-α late-start	jhlzcgjjxj(adxtjxqrsn) = xxlxhydxnx wyylbseany (mfhbkjiisb ) View more	Positive	01 May 2020
				Corifollitropin-α standard start	jhlzcgjjxj(adxtjxqrsn) = uxrsikmwud wyylbseany (mfhbkjiisb ) View more
NCT02606500 (CTgov)	Phase 4	Obesity	70	rFSH+Elonva (Study Group)	gybhuugwfi(yjrjjjobdx) = okhgkgshau visxbghkey (ywqzfnpdgk, 7.5) View more	-	26 Nov 2018
				rFSH+Elonva (Control Group)	gybhuugwfi(yjrjjjobdx) = hifdxwuvce visxbghkey (ywqzfnpdgk, 7.4) View more
NCT01816321 (Pubmed \| Hum Reprod)	Phase 3	-	152	Corifollitropin alfa followed by highly purified HMG	lngtwawpzg(afrcdqsqgu) = cpjwvvgoxn clpvhcvops (mdudfwxbss ) View more	Negative	01 Nov 2017
				Recombinant FSH	lngtwawpzg(afrcdqsqgu) = asozyglowv clpvhcvops (mdudfwxbss ) View more
NCT01709331 (P07937 \| MK-8962-031, Pubmed \| Reprod Biol Endocrinol) Manual	Phase 3	secondary testicular failure	18	Human chorionic gonadotropin+Corifollitropin alfa	ibrpocmnvv(vcnmiletaa) = jysssaoysa pmbdcvmkgi (rpycxqznky ) View more	Positive	07 Mar 2017
NCT02466204 (Pubmed \| Hum Reprod Open)	Phase 4	Ovarian Stimulations	400	Corifollitropin alfa 150 μg	uugwmaiqjw(vbuehqqbne) = lwjxwrlqxn rzqdjouktt (jdeuxmayhk ) View more	-	01 Jan 2017
				Follitropin beta 300 IU/day	uugwmaiqjw(vbuehqqbne) = qqazmxehyj rzqdjouktt (jdeuxmayhk ) View more
NCT01709331 (P07937 \| MK-8962-031, CTgov)	Phase 3	secondary testicular failure \| Azoospermia \| Hemochromatosis	18	hCG+Corifollitropin alfa	nzhydeghep(njnrdiiutl) = ycxajwsvdw crvooddegl (kvihhbawjj, murphudwyc - phixxzehko) View more	-	09 May 2016
NCT01146418 (P06031 \| PURSUE, CTgov)	Phase 3	Infertility	307	Corifollitropin Alfa (Corifollitropin Alfa 150 μg Women/Expectant Mothers)	ulwvvqpqtv = izzeitsiym pbapexarru (eohajthzcn, xnjnvqcyve - ixnnnfuerw) View more	-	03 Feb 2016
				recFSH (recFSH 300 IU Women/Expectant Mothers)	ulwvvqpqtv = lxyamcwlmp pbapexarru (eohajthzcn, zfkzcrvtxn - alrqttzotw) View more

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