Drug Database
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Gensci-004 (PEG rhGH / Gensci 004 / PEG Somatropin)

✓ Approved

GeneScience Pharmaceuticals Co., Ltd. · GHR · Small Molecule

What is Gensci-004?

Gensci-004 is a small molecule developed by GeneScience Pharmaceuticals Co., Ltd.. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesPEG rhGH, Gensci 004, PEG Somatropin
CompanyGeneScience Pharmaceuticals Co., Ltd.
Drug ClassSmall Molecule, Recombinant Proteins
Molecular TargetGHR,
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, GeneScience Pharmaceuticals Co., Ltd.

Mechanism of Action

Molecular Targets

Gensci-004 acts on 2 molecular targets:

GHRgrowth hormone receptor (GHBP, GHIP)
(TERG_01127)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

Gensci-004 is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Endocrine disordersGrowth hormone deficiency✓ Approved

Related Research Articles

PubMedRheumatology international2026-05-24

Sex differences in physical activity, psychosocial determinants, and symptom outcomes in knee osteoarthritis: a cross-sectional analysis of a Hispanic/Latino-predominant cohort.

Jahn Jacob J, Rizk Ryan C RC, Travis Levi M LM, Kholodovsky Eric E et al.

Knee osteoarthritis (KOA) is a chronic disease that often leads to persistent pain, functional limitations, and diminished quality of life. Physical activity can be an effective countermeasure but its adherence typically relies on behavioral determinants. Currently, there is limited work investigating how clinical symptoms among patients with KOA affect behavioral determinants, and there is a need for further insight into why females engage in less physical activity. The purpose of this study was to investigate these questions in a sample of patients with KOA. Patients (n = 736; mean age 56.4 years) with symptomatic KOA (Kellgren-Lawrence grades 0-4) were evaluated at a tertiary sports medicine clinic and completed validated measures of physical activity behavior and behavioral determinants (attitudes, exercise self-efficacy, social support, barriers), in addition to pain and symptoms. Physical activity score was inversely associated with pain intensity (VAS; β = -0.037, p= .004), pain catastrophizing (PCS; β = -0.124, p = .004), and functional limitation (WOMAC; β = -0.364, p < .001). Greater social support was associated with lower WOMAC (β = -.30, p < .001), lower VAS (β = -.14, p =.021), and lower PCS scores (β = -.18, p = .002). Higher exercise self-efficacy was independently associated with reduced pain catastrophizing (PCS; β = -.061, p = .017) and functional limitation (WOMAC; β = -.267, p < .001). Worsening functional status (WOMAC) was significantly associated with more negative affective attitudes (β = .19, p = .001), lower exercise self-efficacy (β = .34, p < .001), and greater perceived barriers (β = .16, p = .002). Exercise intention was a significant predictor of physical activity (β = .36, p <.001), and was itself predicted by affective attitude, social support, self-efficacy, and perceived barriers. Sex comparisons revealed that males scored significantly higher than females in physical activity (p = .015), exercise intention (p = .031), exercise self-efficacy (p = .007), and social support (p = .038), with no significant differences in affective attitude or perceived barriers. Males also reported lower symptom severity than females across VAS (p = .006), PCS (p = .007), and WOMAC (p < .001); however, sex differences in VAS were no longer significant after covariate adjustment.Conclusions. Higher physical activity levels were associated with lower pain and improved functionality in patients with KOA. Sex-based discrepancies in exercise self-efficacy, social support, and exercise intention could help explain why females with KOA participate in less physical activity compared with their male counterparts.

PMID 42176097
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PubMedJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society2026-05-24

Lung mucus burden and treatment response assessed by MRI in the post-modulator era.

Matheson Alexander M AM, Prather Evan E, Willmering Matthew M MM, Mata Jaime J et al.

Mucus is believed to be central to the progressive nature of cystic fibrosis lung disease. Poor clearance leads to plugging, inflammation, and infection, driving a cycle that eventually results in irreversible lung damage. We hypothesized that patients with higher mucus burden would demonstrate greater improvement in spirometry and ventilation when treated with modulator therapy. We retrospectively analyzed data collected in 29 participants prior to and following initiation of elexacaftor/tezacaftor/ivacaftor (ETI) therapy. Participants performed 1H and 129Xe MRI, multiple breath washout tests, and spirometry. Structural abnormalities were quantified using a modified Brody scoring system. 129Xe MRI abnormalities were measured by ventilation defect percent (VDP). Participants with greater mucus burden (the top half, modified Brody score >2.5) showed improved FEV1 (ΔFEV1=10%pred, p=.003), VDP (ΔVDP=-5.6%, p=.004), and lung clearance index (ΔLCI=-1.6, p=.008). Baseline mucus correlated with VDP (ρ=0.48, p = 4e-3), bronchial wall thickening (ρ=0.47, p=.03), and bronchiectasis (ρ=0.80, p = 4e-8). Baseline mucus scores (AUC=0.66) and VDP (AUC=0.75) were associated with lung function improvement (ΔFEV1≥5%pred) following modulator therapy. Functional lung improvement following therapy was related to baseline mucus burden, indicating improved mucus clearance potentially drives better lung function in people receiving ETI therapy. MRI lung mucus scores and regional ventilation were both sensitive biomarkers and likely valuable secondary treatment outcomes in future gene therapies or clinical trials.

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PubMedJournal of veterinary internal medicine2026-05-24

Evaluation of clinical, ultrasonographic, and clinicopathological findings in dogs with pituitary-dependent hypercortisolism and poor trilostane response.

Golinelli Stefania S, Fracassi Federico F, Del Baldo Francesca F, Oliveira Leal Rodolfo R et al.

Trilostane is the treatment of choice for pituitary-dependent hypercortisolism (PDH) in dogs, but predictors of a poor response are unclear. To identify variables associated with a poor response to trilostane in dogs with PDH. Twenty-three dogs with PDH treated with trilostane. Retrospective cohort study. Clinical, clinicopathological, endocrine, ultrasonographic, and treatment data were reviewed. Dogs were classified as good responders (GRs) or nonresponders (NRs) based on clinical outcomes after 4-8 months of trilostane treatment. The primary outcome was treatment response. Fifteen dogs were GRs and 8 were NRs. At diagnosis, GRs had lower alanine aminotransferase (ALT) (median [IQR] 182 [70-251] vs 330 [224-578] U/L; P = .004), eACTH (14.4 [9.25-29.13] vs 49.2 [34.35-62.35] pg/mL; P = .007), and pre-ACTH cortisol (4.28 [3.07-6.52] vs 9.0 [6.57-19.40] μg/dL; P = .019) than NRs. Bilateral adrenomegaly was more frequent in NRs (8/8) than in GRs (9/15; P = .007). At T1, NRs required more rechecks (median [IQR] 7 [6-7] vs 3 [3-5]; P < .001) and higher trilostane doses (3.25 [3-5.75] vs 1.22 [0.66-1.60] mg/kg q12h; P < .001). After false discovery rate adjustment, ALT, eACTH, alopecia, and bilateral adrenomegaly remained significant (q = 0.047 for each). All GRs achieved complete clinical resolution within 4 months of treatment initiation. Higher baseline ALT, eACTH, and pre-ACTH cortisol, as well as bilateral adrenomegaly, were associated with a poor response to trilostane. A lack of improvement by 4-8 months and the need for higher doses or more rechecks supports early therapeutic reassessment.

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PubMedScientific reports2026-05-24

Semantic embedding of variant effect annotations enables rapid and accurate pathogenicity prediction with VUS.Life.

Wu Jiawei J, Stutzman Marissa M, Muriello Michael M, Lincoln Joy J et al.

Interpreting the pathogenicity of genetic variants remains a critical bottleneck in genomic medicine. Millions of variants of uncertain significance (VUS) hinder the clinical application of genetic findings. Traditional computational approaches often rely on hand-engineered features and fail to capture the complexity of multidimensional genomic annotations fully. We developed VUS.Life, a multi-modal framework that synergizes semantic text embeddings of biological and clinical annotations with protein language modeling. We transformed variant annotations from Variant Effect Predictor (VEP) into natural language descriptions which are then converted into vector embeddings via established Large Language Models (LLMs), namely all- mpnet-base-v2, MedEmbed-large-v0.1, and text-embedding-004. Pathogenicity of a variant of interest is predicted by its proximity in the vector embedding space with variants of known pathogenicity. We further extended VUS.Life by employing residue-level delta embeddings from the ESMC-600 M model to capture both clinical context and biophysical constraints. We evaluated the framework on > 10,000 variants across eight ACMG Tier 1 disease genes (BRCA1, BRCA2, FBN1, ATM, PALB2, MYH7, USH2A, and PAH), achieving Leave-One-Out Cross-Validation (LOO-CV) MCC of 0.895-0.989 and F1 ≥ 0.94 across all genes evaluated. Additionally, our unsupervised FBN1 structural analysis using ESMC-600M revealed that delta embeddings disentangled distinct pathogenic mechanisms, topologically separating disulfide bond disruptions from calcium- binding defects. These structural clusters correlated strongly with Zero-Shot Log-Likelihood Ratio (LLR) scores, validating evolutionary fitness as a proxy for pathogenicity. An ablation study removing all pre-computed pathogenicity scores demonstrated that MPNet embeddings retain full discriminative power, confirming that the classifier captures biological signal independent of existing scoring tools. This semantic embedding framework, VUS.Life, accurately captures pathogenicity-relevant features from complex variant annotations, enabling robust automated classification across eight ACMG Tier 1 disease genes and three embedding models. The approach generalizes beyond well-curated genes and supports scalable, interpretable, and representation-based classification of VUS. It holds significant promise for alleviating the variant interpretation bottleneck in clinical genomics.

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PubMedInternational journal of epidemiology2026-05-24

Comorbidity of asthma and attention deficit hyperactivity disorder in childhood: causal, shared early-life risk factors, or shared genetic liability?

Talaei Mohammad M, Pagoni Panagiota P, Stergiakouli Evie E, Shaheen Seif O SO

The positive association between childhood asthma and attention deficit hyperactivity disorder (ADHD) has not been adequately explained. We aimed to investigate whether it is causal or whether shared genetics and/or shared early-life risk factors explain the link. We used a two-sample Mendelian randomization (MR) to test whether there is a causal relationship between asthma and ADHD. In the Avon Longitudinal Study of Parents and Children (ALSPAC), we defined doctor-diagnosed asthma, its endotypes according to atopy determined by skin-prick tests, and the risk of ADHD by using the Strengths and Difficulties Questionnaire, all at 7 years of age. We explored whether the asthma-ADHD association was attenuated when controlling for an extensive number of early-life risk factors (N = 7165). Child polygenic risk scores (PRSs) for asthma and ADHD were calculated by using published genome-wide association studies across seven P-value thresholds (<5 × 10-8 to <.5) (N = 5425-5503). We found little evidence of a causal effect between asthma and ADHD in both directions. In ALSPAC, asthma [odds ratio (OR) 1.35, 95% confidence interval (CI) 1.10 - 1.65], particularly non-atopic asthma (OR 1.51, 95% CI 1.09 - 2.08), was associated with ADHD in crude models, while atopic asthma was not (OR 1.00, 95% CI 0.69 - 1.45). These associations were largely attenuated after adjusting for 15 shared early-life risk factors (OR 1.14, 95% CI 0.92 - 1.41 for asthma and OR 1.24, 95% CI 0.88 - 1.74 for non-atopic asthma). There was little evidence of association between asthma PRSs and ADHD at any P-value threshold. We found evidence of an association between ADHD PRSs and asthma and non-atopic asthma at most thresholds; the strongest association was at P < 5 × 10-3 (OR 1.12, 95% CI 1.04 - 1.22, P = .004) for asthma and at P < 5 × 10-2 (OR 1.18, 95% CI 1.04 - 1.34, P = .01) for non-atopic asthma. The association between asthma and ADHD in childhood is unlikely to be causal and is largely explained by shared early-life risk factors, with some evidence for a shared genetic background.

PMID 42176346
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PubMedMedicine2026-05-23

Propensity score matching analysis of the association between Helicobacter pylori infection and colorectal polyps: A case-control study.

Gong Yating Y, Fan Zhen Z

The association between Helicobacter pylori (H. pylori) infection and colorectal polyps remains controversial. This study was a retrospective observational study. A total of 1106 patients who underwent gastrointestinal endoscopy at the First People's Hospital of Fuyang from January 2021 to May 2023 were enrolled. Based on colonoscopic findings, patients were stratified into a colorectal polyp group (n = 401) and a control group (n = 705). Propensity score matching (PSM) was applied in a 1:1 ratio to balance baseline confounders. Conditional logistic regression evaluated the association between H. pylori infection and colorectal polyps. Before PSM, significant differences were observed in body mass index, age, male sex, alcohol consumption history, smoking history, diabetes mellitus, and hypertension between the colorectal polyp group and control group (P < .05). After PSM, 347 matched pairs were generated. Using the matched sample, conditional logistic regression analysis identified H. pylori infection as a risk factor for colorectal polyps (odds ratio = 1.65, 95% confidence interval [CI]: 1.17-2.33; P = .004). Receiver operating characteristic curve analysis yielded an area under the curve of 0.549 (95% CI: 0.506-0.592; P = .025) for H. pylori infection in predicting polyps. The application of PSM further validates the association between H. pylori infection and colorectal polyps. H. pylori infection alone demonstrates limited predictive utility for colorectal polyp risk.

PMID 42175495
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