Drug Database
LH

LH + FSH (Menopur / LH + FSH, Ferring / Meropur)

✓ Approved

Ferring · FSHR

What is LH + FSH?

LH + FSH is a therapeutic agent developed by Ferring. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection or subcutaneous injection.

Drug Profile

Brand NamesMenopur, LH + FSH, Ferring, Meropur
CompanyFerring
Molecular TargetFSHR, LHCGR
RouteInjectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Ferring

Mechanism of Action

Molecular Targets

LH + FSH acts on 2 molecular targets:

FSHRfollicle stimulating hormone receptor (FSHRO, ODG1)
LHCGRluteinizing hormone/choriogonadotropin receptor (ULG5, LH/CGR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

LH + FSH is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Reproductive system and breast disordersInfertility female✓ Approved

Related Research Articles

PubMedJournal of pediatric endocrinology & metabolism : JPEM2026-08-25

Clinical, hormonal, and genetic spectrum of cryptorchidism: a comprehensive evaluation of patients referred for pediatric endocrinological assessment.

Sütçü Zümrüt Kocabey ZK, Kaplan Emel Hatun Aytaç EHA, Önal Hasan H

Cryptorchidism is the most prevalent pediatric genital anomaly, yet its clinical significance often extends beyond simple anatomical maldescent. While surgical management is well-established, the necessity for holistic endocrine and genetic evaluation remains underexplored. We aimed to characterize the clinical, hormonal, and genetic landscapes of patients referred for pediatric endocrinological assessment following orchiopexy. We retrospectively analyzed 99 boys referred for postoperative evaluation. Clinical findings, basal and dynamic hormonal profiles, and genetic results - including karyotype and targeted DSD gene panels - were evaluated. Preterm birth was recorded in 23.2 % of the cohort, and bilateral involvement was present in 50.5 %. Significant clinical findings included testicular atrophy (34.3 %), scrotal hypoplasia (18.2 %), micropenis (12.1 %), and hypospadias (10.1 %). Hormonal profiling revealed a broad spectrum of FSH (up to 85.7 mIU/mL) and AMH (0.01-71.80 ng/mL) levels. Among patients undergoing hCG stimulation testing, 72.7 % exhibited an insufficient testosterone response. Targeted DSD panel testing in a selected high-risk subgroup yielded a diagnostic rate of 45.4 %, identifying variants in SRD5A2, PTPN11, NR0B1, RAF1, POR, LHX4, and AMHR2. The prevalence of nonisolated cryptorchidism was relatively high, affecting 44.4 % of the cohort. This multisystemic involvement comprised defined syndromic diagnoses (17.2 %) and chronic comorbidities (27.3 %), predominantly endocrine disorders such as congenital hypothyroidism and growth hormone deficiency. The high frequency of bilateral involvement, testicular atrophy, and genetic mutations suggests that many referred cases represent complex syndromic or endocrine conditions rather than isolated maldescent. Comprehensive endocrinological follow-up and targeted genetic testing are essential for early diagnosis and optimizing long-term fertility management.

PMID 42638530
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PubMedJournal of the Endocrine Society2026-08-24

Hormonal profiles of men with highly elevated SHBG and primary testicular dysfunction support free hormone hypothesis.

Gagliano-Jucá Thiago T, Puri Ishika I, Ramirez-Rivera Gabriel G, Shekhar Skand S et al.

Free hormone hypothesis (FHH) posits that free testosterone crosses plasma membrane to activate intracellular signaling and is biologically active fraction of circulating testosterone. Widely accepted in other fields, FHH has been debated in andrology. To disentangle the roles of free and total testosterone, we studied men with greatly elevated sex hormone-binding globulin (SHBG) levels and primary hypogonadism, who had marked divergence in total and free testosterone concentrations, in whom elevated gonadotropins provided independent evidence of primary testicular insufficiency. Prospective hormonal evaluation of men with greatly elevated SHBG. Total and free testosterone, LH, FSH, symptom ascertainment. Among 20 men with SHBG>100 nmol/L, 15 met Endocrine Society's criteria for primary hypogonadism: low free testosterone, one or more symptoms/signs, elevated LH and/or FSH. Among 15 men with elevated LH and/or FSH and unequivocally low free testosterone who met the criteria for primary hypogonadism, 4 had total testosterone that exceeded the reference range (>916 ng/dL) and 8 had total testosterone >450 ng/dL, substantially above the lower normal limit. In men with markedly elevated SHBG, in whom total and free testosterone diverged substantially, low free testosterone was associated with elevated gonadotropins, providing independent evidence of primary testicular insufficiency even when total testosterone levels were above the reference range or substantially above the lower normal limit. Although sample size was small, these illustrative "n-of-1" observations in uncommon patients are consistent with the primacy of free testosterone over total testosterone in the hypothalamic-pituitary-testicular feedback loop to regulate LH and FSH, and support the FHH.

PMID 42634762
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PubMedCureus2026-08-24

Case Report of Initial Manifestation of Hypogonadotropic Hypogonadism Based on Unoccluded Growth Plates in a 26-Year-Old Vietnamese Patient.

Lehnert Richard R, Buschhart Anna-Lena AL, Schultz Emanuel E, Schneider Stephanie S et al.

Hypogonadotropic hypogonadism is a rare endocrine disorder characterized by deficient secretion of gonadotropin-releasing hormone (GnRH), leading to reduced levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), ultimately resulting in impaired sexual maturation and pubertal development. While typically diagnosed during adolescence, rare cases present in adulthood as incidental findings. This case report describes an unusual presentation of hypogonadotropic hypogonadism discovered incidentally during treatment of a traumatic tibial fracture in a 26-year-old male patient, highlighting the importance of recognizing unoccluded growth plates as a potential indicator of underlying endocrine pathology. A 26-year-old Vietnamese male (height 1.70 m, weight 59 kg, BMI 20.4 kg/m²) presented to the emergency department on December 27, 2022, with left lower leg pain following a work-related accident. Radiographic imaging revealed a spiral fracture of the left tibial shaft with notably unoccluded growth plates. Physical examination demonstrated absent secondary sexual characteristics, including lack of pubic hair and prepubertal genitalia. The patient reported no previous medical conditions or current medications, though his history included mumps at age 10, raising the possibility of orchitis. Serial laboratory measurements over three consecutive days (at 8:45 AM each day) revealed consistently low serum testosterone (15.0-20.0 ng/dL; reference: 249-836 ng/dL), LH (0.17-0.22 IU/L; reference: 1.70-8.60 IU/L), and FSH (0.66-0.69 IU/L; reference: 1.50-12.4 IU/L), confirming the diagnosis of hypogonadotropic hypogonadism. Other pituitary function tests were within normal limits. The tibial fracture was treated with closed reduction and intramedullary interlocking nail fixation. Following endocrinological consultation, the patient was initiated on testosterone replacement therapy administered every three months. This case demonstrates an uncommon adult presentation of hypogonadotropic hypogonadism diagnosed incidentally following traumatic injury. The presence of unoccluded growth plates on routine radiographic imaging in an adult patient served as a crucial diagnostic clue, emphasizing the importance of systematic evaluation of skeletal maturity and endocrine status when such findings are encountered. Early recognition and appropriate hormonal replacement therapy are essential for addressing both the endocrine deficiency and potential skeletal complications. Long-term follow-up will determine the effectiveness of testosterone therapy and whether growth plate closure can be achieved.

PMID 42634669
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PubMedProtein science : a publication of the Protein Society2026-08-24

Structural and biophysical characterization of Mycobacterium tuberculosis DciA reveals functional convergence in DnaB helicase recognition.

Mazzoletti Daniele D, Garavaglia Andrea A, Fisher Hayden H, Gao Nicholas N et al.

In bacteria, DnaB replicative helicases are essential for unwinding genomic DNA to provide the single-stranded templates required for replication. The recruitment of the hexameric DnaB helicase to the origin of replication is mediated by distinct mechanisms that rely on specialized factors known as helicase loaders. The DciA family of helicase loaders exhibits distinct architectures that differ in the arrangement of the KH and DnaB-binding lasso domains. In this study, we probe the predicted structural architecture of the Mycobacterium tuberculosis (Mt) DciA helicase loader and its interplay with the cognate helicase MtDnaB. Native mass spectrometry and small-angle X-ray scattering (SAXS) analyses reveal that MtDciA adopts a monomeric and compact architecture in solution. We demonstrate that MtDnaB binds MtDciA with nanomolar affinity, likely forming a 2:1 complex at the Docking Helix-Linker Helix (DH-LH) interface of the replicative helicase. We predict that the intein-containing immature MtDnaBi will fail to form the active hexamer. As such, we suggest that MtDciA will show little to no affinity for intein-containing MtDnaBi.

PMID 42635293
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PubMedJournal of neuroendocrinology2026-08-23

Comparative analysis of SCGN expression patterns in the anterior pituitary gland of mouse, pig, and human by single-cell transcriptomics.

Wang Cheng-Cheng CC, Zhang Qi-Lin QL, Zang Zhen-Le ZL, Yin Hua-Chun HC et al.

Secretagogin (SCGN) is a calcium-binding protein implicated in neuroendocrine secretion. However, its expression profile in the anterior pituitary gland and potential species-specific differences remain poorly characterized. We analyzed scRNA-seq data from the pituitary glands of mice, rats, pigs, and humans, then combined it with validation by immunostaining to systematically elucidate the expression and distribution patterns of SCGN in the anterior pituitary gland. SCGN exhibited distinct species-specific expression patterns. In mice, SCGN transcripts were predominantly enriched in PIT1-lineage lactotropes and SF1-lineage gonadotropes, with immunofluorescence confirming high colocalization with LH, FSH, and PRL. In pigs, SCGN was primarily expressed in TPIT-lineage corticotropes, and immunofluorescence colocalization analysis confirmed the highest colocalization rate with ACTH. In humans, SCGN expression was confirmed in the anterior pituitary gland by immunohistochemistry, while scRNA-seq revealed predominant enrichment of its transcripts in PIT1-lineage lactotropes and somatotropes. Notably, comparative interspecies analysis indicated a high degree of similarity in SCGN enrichment within PIT1-lineage cells (particularly lactotropes) between mice and humans. In contrast, SCGN expression was undetectable in the rat anterior pituitary gland at both transcriptional and protein levels. Together, our findings suggest that SCGN may not be an essential or universal regulator of anterior pituitary hormone secretion. Instead, this study provides an informative negative example that highlights the interspecies divergence of the pituitary secretory machinery among mammals.

PMID 42633787
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PubMedJournal of reproduction & infertility2026-08-23

Successful Intrauterine Insemination Following Estradiol Pretreatment in a Patient with Primary Ovarian Insufficiency: A Case Report.

Huynh Trang Nguyen Khanh TNK, Huynh Minh Phuc Khanh MPK, Ly Loc Thai LT

Premature ovarian insufficiency (POI) is a clinical condition characterized by impaired ovarian function to secrete gonadal hormones, leading to hypoestrogenism and amenorrhea before the age of 40. Oocyte depletion in POI significantly reduces the chance of spontaneous conception, making infertility a key concern. Various in vitro fertilization (IVF) stimulation protocols, including estrogen pretreatment, have been investigated to facilitate conception with autologous oocytes in patients with POI. The principle of estrogen pretreatment involves administering exogenous estrogen to suppress elevated pituitary gonadotropins (FSH and LH), thereby restoring normal follicular development. This article presents a case of a 32-year-old patient with POI, characterized by severely diminished ovarian reserve, as evidenced by an AMH level of 0.03 ng/ml and an antral follicle count (AFC) of 1. Our patient had been attempting to conceive for 14 months and reported shortened menstrual cycles. Hysterosalpingography revealed bilaterally patent fallopian tubes, and the patient's partner demonstrated normozoospermia. The patient was initially scheduled for IVF with controlled ovarian stimulation and estrogen pretreatment. However, a spontaneously matured follicle was detected during the course of estrogen therapy. Consequently, the patient was advised to undergo intrauterine insemination (IUI) following ovulation triggering with human chorionic gonadotropin (hCG). The procedure resulted in a clinical pregnancy and culminated in a term live birth. In POI patients using for estrogen pretreatment autologous oocytes, may enhance ovarian responsiveness. If a mature follicle emerges during estrogen pretreatment, ovulation induction with IUI offers a viable path to natural conception.

PMID 42633041
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