Drug Database
RE

recombinant FSH (FostiRel)

✓ Approved

Reliance Life Sciences Private Limited · FSHR · Recombinant Proteins

What is recombinant FSH?

recombinant FSH is a recombinant proteins developed by Reliance Life Sciences Private Limited. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesFostiRel
CompanyReliance Life Sciences Private Limited
Drug ClassRecombinant Proteins
Molecular TargetFSHR
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Reliance Life Sciences Private Limited

Mechanism of Action

Molecular Targets

recombinant FSH acts on 1 molecular target:

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

Therapeutic Indications

recombinant FSH is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Reproductive system and breast disordersInfertility female✓ Approved

Related Research Articles

PubMedZhonghua nan ke xue = National journal of andrology2026-11-11

[Effect of Guilu Taohong decoction on spermatogenic function and sex hormone levels in a rat model of varicocele].

Yang Yang Y, Wang Biao B, Qiu Zerui Z, Wang Yizhuo Y et al.

Objective To investigate the effects and mechanisms of Guilu Taohong decoction on spermatogenic function and sex hormone levels in a rat model of varicocele (VC). Methods Forty-eight SPF-grade male SD rats (6 weeks old) were randomly assigned to the sham-operated group, model group, Guilu Taohong decoction group and L-carnitine group. Except for the sham operation group, the other groups were respectively given corresponding drug intragastric intervention for 8 weeks after modeling. After the intervention, the diameters of the left spermatic vein in each group of rats were detected. The morphological structure of testicular, epididymal and renal tissues was observed by HE staining, and the degree of testicular interstitial fibrosis was evaluated by Masson staining. The levels of serum testosterone (T), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and inhibin B (INH-B) were detected by ELISA. The expressions of hypoxia-inducible factor-1 α (HIF-1α) and vascular endothelial growth factor A (VEGFA) in testicular tissue were detected by Western blot.Results Compared with the sham-operated group, the left spermatic vein of rats in the model group was significantly dilated (P<0.01), the tissue structure of the testis and epididymis was disordered, spermatogenic cells decreased, and interstitial fibrosis was obvious. The levels of serum T and INH-B decreased significantly (all P<0.01), the levels of FSH and LH increased (all P<0.01), and the expressions of HIF-1α and VEGFA were significantly upregulated (all P<0.01). Compared with the model group, the Guilu Taohong decoction group exhibited significantly reduced left spermatic vein diameter (P<0.05), improved testicular and epididymal structure, increased spermatogenic cell number, attenuated interstitial fibrosis, elevated serum T and INH-B(all P<0.01), decreased FSH and LH levels (all P<0.05), and downregulated HIF-1α and VEGFA expression (all P<0.01). Compared with the sham-operated group，the L-carnitine group showed increased T and INH-B levels (all P<0.05), decreased FSH and LH levels (all P<0.01), and reduced HIF-1α and VEGFA expression (all P<0.05). But Guilu Taohong decoction group exhibited more pronounced T elevation and HIF-1α reduction (P<0.05). The renal tissue structures of rats in each group were intact, and no obvious pathological changes were observed. Conclusions Guilu Taohong decoction effectively improves spermatic vein dilation and spermatogenic function in VC model rats. Its mechanisms may involve inhibition of HIF-1α/VEGFA expression, alleviation of local hypoxia and tissue fibrosis, and restoration of reproductive endocrine homeostasis, with good safety.

PMID 43012206
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PubMedFrontiers in veterinary science2026-11-11

Comparison of the pathogenicity of a Taiwan lineage 1 NADC30/34-like recombinant and a lineage 3 Betaarterivirus suid 2 in pigs.

Lai Yi-Fang YF, Lin Chao-Nan CN, Chiou Ming-Tang MT, Chang Yen-Chen YC et al.

Porcine reproductive and respiratory syndrome virus 2 (PRRSV-2; Betaarterivirus suid 2) causes porcine reproductive and respiratory syndrome, leading to severe economic losses in the global swine industry. Lineage 1 (L1) PRRSV-2 has emerged and become increasingly prevalent in North America and Asia. This study compared the pathogenic characteristics of a Taiwan NADC30/34-like L1 recombinant and a lineage 3 (L3) PRRSV-2 strain and evaluated their suitability for establishing an experimental infection model in growing pigs. Ten-week-old pigs were inoculated with either the NADC30/34-like L1 NPUST-107-844/2018 strain or the L3 SW2018001-YL strain via concurrent intranasal and intramuscular routes. Pigs inoculated with the L1 strain exhibited higher body temperatures and a greater frequency of fever during the early post-inoculation period than those inoculated with the L3 strain. However, no significant differences were observed between the groups in peak viremia, lung pathological scores, or plasma cytokine concentrations. These results indicate that the Taiwan L1 strain induced a more pronounced early febrile response but produced virological, pulmonary pathological, and systemic cytokine responses comparable to those induced by the Taiwan L3 strain. Collectively, these findings highlight the pathogenic diversity of circulating PRRSV-2 strains in Taiwan and for future experimental studies, including investigations of disease pathogenesis, therapeutic interventions, and vaccine development.

PMID 43011046
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PubMedInternational braz j urol : official journal of the Brazilian Society of Urology2026-11-11

Exploring the Association Between Cannabis Use and Male Reproductive Parameters: A Systematic Review and Meta-Analysis.

Marquardt Nilson N, Felkl Otto Rauber OR, Veiga Davi Marçola DM, Pires Iago Zang IZ et al.

This systematic review and meta-analysis evaluated the association between cannabis use and male reproductive function, specifically sperm parameters and serum hormone levels. We searched PubMed, Embase, and the Cochrane Library (August-September 2025) for studies assessing cannabis exposure and male fertility outcomes. Data were pooled using random-effects models, with heterogeneity assessed by I²/Q statistics and publication bias by funnel plots/Egger's test, following PRISMA guidelines (PROSPERO: CRD420251132635). A total of 18 studies (5,766 patients, 6,231 samples; mean age 36.5 ± 9.9 years) were included for sperm outcomes, and 21,066 patients (mean age 37.4 ± 10.4 years) for hormonal outcomes. All cannabis users reported smoking more than one joint per week in the preceding months. Cannabis users showed a significant reduction in sperm morphology compared to non-users (MD = -1.02; 95% CI: -1.93 to -0.10; p < 0.05), which persisted even when restricted to studies strictly following WHO criteria. No significant differences were found for sperm concentration, ejaculate volume, total sperm count, or progressive and total motility. Hormonal analysis revealed no differences in testosterone, FSH, or LH, but SHBG levels were significantly higher in cannabis users (MD = 3.90; 95% CI: 1.67-6.13; p <0.05). These findings suggest that cannabis use should be considered in the lifestyle assessment of men evaluated for subfertility and infertility. Although causality could not be established, cannabis should be considered a potential lifestyle factor, particularly in cases of abnormal sperm morphology or unexplained infertility. Further studies on sperm function are needed to clarify its effects on testicular function and fertilizing capacity.

PMID 43012629
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PubMedVeterinary research2026-11-11

Orf virus early genes ORFV113 and ORFV114 are individually dispensable for replication in vitro but required for full virulence in vivo.

Zhou Weijie W, Hu Jingjin J, Wang Xiaoyue X, Wang Naixiu N et al.

Orf is a highly contagious zoonotic disease caused by Orf virus (ORFV), resulting in significant economic losses to the livestock industry. ORFV113 and ORFV114, located in the terminal variable region of the ORFV genome, are putative virulence-associated genes. To elucidate their biological functions, we characterized the transcription kinetics of both genes and generated single-gene deletion mutants by homologous recombination, using transfer plasmids carrying flanking homology arms and an enhanced green fluorescent protein (EGFP) reporter cassette. Lamb testis (LT) cells transfected with the recombinant plasmids were infected with the parental ORFV-JS strain; recombinant viruses were enriched by limiting dilution, purified by consecutive rounds of plaque isolation, and verified by polymerase chain reaction (PCR). Both genes are highly conserved among ORFV isolates (92-100% nucleotide identity) and are transcribed with early kinetics. The genetically stable deletion mutants, designated ORFV-Δ113 and ORFV-Δ114, were successfully generated. Deletion of either gene did not significantly alter viral growth kinetics or cytopathic effects (CPE) in LT cells. In a rabbit skin scarification model (n = 4 per group), however, both mutants induced markedly milder macroscopic lesions with lower cumulative clinical scores (P < 0.05), and viral loads in scab tissue were reduced 17-fold (ORFV-Δ113) and 10-fold (ORFV-Δ114) relative to the wild-type strain (P < 0.01). Thus, ORFV113 and ORFV114 are dispensable for viral replication in vitro but are required for full virulence in vivo. The resulting deletion mutants provide valuable tools for dissecting virus-host interactions and are promising candidates for the rational design of live-attenuated ORFV vaccines.

PMID 43010051
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PubMedZhonghua yi xue za zhi2026-11-11

[Mechanism of endothelial cell-derived S100A11 in promoting radiation-induced cardiac fibrosis in C57BL/6 mice].

Xie Y X YX, Liao X X, Shen H T HT, Xu W J WJ et al.

Objective: To investigate the role and mechanism of cardiac endothelial cell-derived S100A11 in promoting radiotherapy-induced cardiac fibrosis in C57BL/6 mice. Methods: Eight 6-week-old female C57BL/6 mice were randomly divided into a control group (n=4) and a radiotherapy group (n=4) using a random number table. The control group received no intervention, while the radiotherapy group received a single high-dose irradiation of 16 Gy to the left thorax to establish a mouse model of cardiac injury. At 12 weeks after radiotherapy, echocardiography was performed to measure left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and left ventricular internal dimension at end-systole (LVIDs). Western blotting was used to detect the expression of collagen type Ⅰ (COL Ⅰ) and alpha-smooth muscle actin (α-SMA) in mouse cardiac tissue. The mouse cardiac endothelial cell line MCEC were divided into a control group and a radiotherapy group (medium was replaced after endothelial cell adherence, followed by radiotherapy and continued culture for 24 h before sample collection). The supernatants from the control and radiotherapy endothelial cell groups were mixed with complete medium at a 1∶1 ratio and used to culture primary cardiac fibroblasts extracted from C57BL/6 mouse cardiac tissue. These fibroblasts were divided into a control group and a treatment group. Western blotting was used to detect COL Ⅰ and α-SMA protein expression and a scratch assay was used to assess cell migration ability. Endothelial cells were divided into a control group and a radiotherapy group. Western blotting, quantitative real-time PCR, and enzyme-linked immunosorbent assay (ELISA) were used to detect the expression and secretion of S100 calcium-binding protein A11 (S100A11) in endothelial cells. Small interfering RNA (siRNA) was used to knock down S100A11 gene expression in endothelial cells. Two siRNAs targeting S100A11 and a siRNA negative control group were separately transfected into endothelial cells. Western blotting was used to verify whether S100A11 expression in endothelial cells was successfully knocked down. The S100A11-knockdown endothelial cells were then subjected to radiotherapy and divided into a control group, siRNA-1 group, and siRNA-2 group. The sample collection method and the method for co-culturing primary fibroblasts were the same as described above, with groups designated as control, siRNA-1, and siRNA-2. Western blotting was used to detect COL Ⅰ and α-SMA protein expression. Primary fibroblasts were treated with recombinant S100A11 protein (100 ng/ml) for 24 h, and Western blotting and immunofluorescence were used to detect COL Ⅰ and α-SMA expression. Transcriptome sequencing was used to detect gene expression changes in primary fibroblasts treated with recombinant S100A11 protein for 24 h. Small interfering RNA (siRNA) was used to knock down integrin subunit beta-like 1 (ITGBL1) gene expression in primary fibroblasts. Two siRNAs targeting ITGBL1 (siRNA-1 and siRNA-2) (i.e., the siRNA group) and a siRNA negative control (si-NC) group were separately transfected into primary fibroblasts. Western blotting was used to verify knockdown of ITGBL1 expression in primary fibroblasts. Primary fibroblasts with ITGBL1 knockdown were cultured with recombinant S100A11 protein for 24 h, and Western blotting and immunofluorescence were used to detect COLⅠ and α-SMA protein expression. Results: Compared with the control group, echocardiography showed that LVEF and LVFS were lower in the radiotherapy group (both P<0.001), and COL Ⅰ and α-SMA protein expression levels in cardiac tissue were higher in the radiotherapy group (both P<0.001). Perivascular fibrotic tissue in the hearts of irradiated mice was increased than that of the control group (all P<0.05). The mRNA, protein, and supernatant protein expression of S100A11 in endothelial cells were higher in the radiotherapy group than in the control group (all P<0.001). The supernatant from radiotherapy-treated endothelial cells increased and α-SMA protein expression in primary fibroblasts compared with the control group (all P<0.05). In S100A11-knockdown endothelial cells subjected to radiotherapy, COL Ⅰ and α-SMA protein expression in primary fibroblasts in the siRNA groups were lower than in the control group (all P<0.05). Recombinant S100A11 protein increased COL Ⅰ and α-SMA protein expression in primary fibroblasts compared with the control group (all P<0.05). Transcriptome sequencing indicated that ITGBL1 gene expression levels were higher in primary fibroblasts treated with recombinant S100A11 protein than in the control group. After ITGBL1 knockdown, S100A11 promoted COL Ⅰ and α-SMA protein expression in primary fibroblasts were lower than in the control group (P<0.05). Conclusions: After radiotherapy, S100A11 expression and secretion are increased in cardiac endothelial cells. This effect can further activate cardiac fibroblasts in C57BL/6 mice and promote the development and progression of cardiac fibrosis.

PMID 43010754
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PubMedFrontiers in aging2026-11-11

Maintaining Klotho: preventing the body from unwinding.

Gunzburg Walter H WH, Pawa Pharon P, Salmons Brian B

The Klotho gene, discovered in 1997, encodes a protein that plays a pivotal role in regulating aging and longevity. Reduced Klotho expression is associated with multiple age-related diseases, including renal, cardiovascular, neurodegenerative, and metabolic disorders, leading to the notion that supplementation of the levels of Klotho may have a beneficial, or even a therapeutic, effect. Despite promising early stage results from recombinant and gene-based therapies, clinical translation has been hindered in part by the protein's short half-life as well as the immune clearance of Klotho producing cells. This article reviews Klotho's biological significance and therapeutic challenges, as well as introducing a novel encapsulation-based approach-Cell-in-a-Box® technology-as a proposed potential solution for sustained Klotho delivery. Encapsulated Klotho-producing cells may potentially enable continuous secretion, immune protection, and long-term efficacy, offering a transformative strategy for anti-aging and disease modification.

PMID 43010923
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