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Loxosceles Immune F(Ab)2 (Reclusmyn)

✓ Approved

Instituto Bioclon · Polyclonal Antibodies · Polyclonal Antibodies

What is Loxosceles Immune F(Ab)2?

Loxosceles Immune F(Ab)2 is a polyclonal antibodies developed by Instituto Bioclon. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesReclusmyn
CompanyInstituto Bioclon
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Instituto Bioclon

Therapeutic Indications

Loxosceles Immune F(Ab)2 is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Injury, poisoning and procedural complicationsVenom poisoning✓ Approved

Related Research Articles

PubMedGenes & diseases2026-09-20

Autosomal dominant gain-of-function mutations in LCP1 cause a syndromic neutropenia and immunodeficiency.

Yu Lang L, Zhou Bo B, Liu Wei W, Li Wenhui W et al.

Actin cytoskeleton defects underlie immuno-actinopathies. We identified three patients with heterozygous LCP1 gain-of-function mutations (L362F, A365D) causing activated LCP1-associated immunodeficiency syndrome, characterized by congenital neutropenia, variable combined immunodeficiency, and allergy. Patients' neutrophils show maturation arrest and excessive apoptosis, while T/B cells are reduced and functionally impaired. Patient-derived iPSCs, CRISPR-edited cells, and LCP1+/L362F mice replicate these defects. Mechanistically, mutant LCP1 hyper-bundles F-actin, inducing VDAC1 oligomerization and mitochondrial apoptosis. This study further establishes LCP1 as a regulator of immune cell fate and suggests targeting actin dynamics as therapy.

PMID 42763497
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PubMedClinical neurophysiology practice2026-09-20

Cathodal tDCS in obsessive-compulsive disorder: cognitive and neurophysiological outcomes in a double-blind sham-controlled trial.

Zaks-Ohayon Rut R, Hakmon Talia Beit-On TB, Cohen Hagit H, Besser Itay I et al.

This preliminary study examined the efficacy of cathodal transcranial direct current stimulation (tDCS) targeting the medial prefrontal cortex (mPFC) in reducing symptom severity, enhancing cognitive flexibility, and modulating brain-derived neurotrophic factor (BDNF) levels in individuals with obsessive-compulsive disorder (OCD). A double-blind, randomized, sham-controlled trial was conducted with 20 patients meeting DSM-V criteria for OCD, of whom 15 completed the intervention and were included in the final analysis. Participants received cathodal mPFC-tDCS (2 mA, 20 min, 10 sessions) or sham stimulation. Symptom severity (Y-BOCS), cognitive flexibility (task-switching), salivary BDNF, and frontal alpha activity (qEEG at Fz) were measured at baseline, post-treatment, and follow-up. The tDCS group exhibited greater reductions in Y-BOCS scores over time (F(2, 26) = 12.562, p < 0.001, partial η2 = 0.425). Task-switching performance improved in the experimental group compared with controls (F(2, 26) = 20.351, p < 0.001, partial η2 = 0.531). Salivary BDNF levels increased significantly in the tDCS group at follow-up (F(2, 16) = 6.086, p = 0.01, partial η2 = 0.432). Trends toward normalization of frontal alpha activity were observed, but did not reach statistical significance. Cathodal mPFC-tDCS was associated with reduced OCD symptom severity, improved cognitive flexibility, and increased salivary BDNF. These preliminary findings warrant replication in larger controlled samples. This study extends previous tDCS research in OCD by integrating clinical outcomes with cognitive performance and a peripheral marker of neuroplasticity. It provides preliminary support for mPFC-targeted tDCS as a potential intervention for OCD.

PMID 42763492
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PubMedGenes & diseases2026-09-20

ZO-2 blocks the localization of PGAM5 protein to the mitochondrial membrane and suppresses pancreatic cancer malignancy through metabolic reprogramming.

Yu Sen S, Ke Mingxin M, Ma Muyuan M, Jiang Tingting T et al.

Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related death with limited treatment options, and there is an urgent need to develop effective therapeutic strategies. The zonula occludens-2 (ZO-2) protein is a member of the tight junction protein family, and its function and underlying mechanisms of action in PDAC are unknown. Gene expression and its association with the clinicopathologic characteristics of patients with PDAC were analyzed using immunohistochemistry and bioinformatics and functionally validated by using in vitro and in vivo mouse models. Protein expression and protein regulation were measured by using gain- and loss-of-function assays and molecular biology methods. The expression level of ZO-2 decreased in PDAC and was highly correlated with aggressive pathological features and the prognosis of patients. Increased expression of ZO-2 inhibited the proliferation, migration and colony formation of PDAC cells in vitro and inhibited PDAC tumor growth and liver metastasis in vivo. Mechanistically, ZO-2 bound to the mitochondrial membrane protein phosphoglycerate mutase 5 (PGAM5) and trapped it in the cytosol. Reduced expression of ZO-2 caused increased mitochondrial localization of PGAM5, leading to activated mitochondrial function and increased intracellular reactive oxygen species and ATP levels, thereby promoting PDAC malignancy, whereas increased ZO-2 expression did the opposite. ZO-2 expression also correlated directly with immune cell infiltration and immune signaling in PDAC. Downregulation of ZO-2 caused increased localization of PGAM5 to the mitochondrial membrane and promoted PDAC malignancy through metabolic reprogramming. ZO-2 is associated with the PDAC immune microenvironment. The ZO-2-PGAM5 axis could serve as a potential therapeutic target in PDAC.

PMID 42763477
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PubMedLogopedics, phoniatrics, vocology2026-09-20

Evaluation of the usability and usefulness of the vocal'iz mobile application in a population of teachers.

Al Rehaoui Racha R, Remacle Angélique A

Although mobile health (mHealth) tools for vocal health are increasingly used, their scientific evaluation remains limited. To assess the perceived usability and usefulness of the Vocal'iz mobile application among teachers. To examine the relationships between these outcomes and individual factors such as age, Voice Handicap Index (VHI-30), health literacy, and digital literacy. Thirty teachers participated in the three phases of our study: (1) completion of a personal data questionnaire, the VHI-30, the Health Literacy Scale, and the Digital Literacy Scale; (2) 10 days of independent use of the application; and (3) completion of the System Usability Scale (SUS) and section F of the Mobile App Rating Scale (MARS) to assess the app's usability and perceived usefulness. A one-sample t-test compared the participants' SUS score to the reference value of 70. A Wilcoxon signed-rank test compared the MARS section F score to the reference value of 3. Correlation tests were conducted between the SUS and MARS scores and the individual factors. The mean SUS score (76.67, SD = 11.55) and the mean score for MARS section F (4.03, SD = 0.74) were both significantly higher than the reference values, with medium to large effect sizes. There were no significant correlations between usability or usefulness and the individual factors. The findings suggest that teachers rated the Vocal'iz app highly, demonstrating its good usability and positive perceived usefulness. The app's potential as a preventive tool warrants further evaluation in more diverse and larger populations, as well as an assessment of its effectiveness.

PMID 42763446
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PubMedMolecular psychiatry2026-09-20

Nociceptin orphanin F/Q Pathways are dysregulated by stress and modulate reward responsiveness and motivated behavior across species.

Pizzagalli Diego A DA, Gallo Meghan M, Treadway Michael T MT, Kangas Brian D BD et al.

Nociceptin orphanin F/Q has been implicated in stress-related depressive phenotypes. Specifically, exposure to chronic stressors upregulates nociceptin receptors (NOPR), whereas NOPR antagonism has antidepressant/anti-anhedonic effects. However, the mechanisms underlying reward-related effects remain unclear. Here, we investigated the role of NOPR in a broad spectrum of reward-related phenotypes (reward consumption, reward learning, motivated behavior) alongside potentially prohedonic effects of NOPR antagonism across species. Study 1 evaluated whether exposure to early-life adversity upregulated ventral tegmental area (VTA) and striatal prepronociceptin (Pnoc) gene expression in adult mice. Study 2 assessed whether NOPR antagonism boosted reward learning in rats using the touchscreen-based Probabilistic Reward Task. Finally, Study 3 tested whether NOPR antagonism modulated decision about motivated behavior using the Effort Expenditure for Reward Task among depressed humans. In Study 1, early-life adversity induced reduced sucrose preference and produced enduring and sex-dependent alterations in effort-related reward behavior, and increased Pnoc expression in the VTA; in females (but not males), early-life adversity increased Pnoc expression in the dorsal striatum. In Study 2, acute administration of 30 mg/kg (but not lower doses) of a NOPR antagonist (BTRX-246040) enhanced reward learning in rats. Finally, in Study 3, relative to placebo, 8-week treatment with BTRX-246040 modulated choice consistency during a motivated task in depressed humans. Collectively, our findings indicate that chronic stress alters Pnoc and mRNA levels of Pnoc-expressing cells in a sex-selective and region-specific manner impacting reward structures, and that NOPR antagonism shows promising efficacy in increasing reward-related behaviors in rodents and humans. Future studies using similar manipulations and outcome measures across species are warranted.

PMID 42763342
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PubMedMolecular psychiatry2026-09-20

Targeting the dopaminergic midbrain with precision 7-Tesla biofeedback training in depression: A proof-of-principle randomized controlled trial.

Morris Laurel S LS, Beltrán Jacqueline M JM, Kvamme Timo L TL, Chowdhury Avijit A et al.

The significant heterogeneity of major depressive disorder (MDD) requires the development of interventions that directly target underlying cognitive or neurobiological mechanisms. This work tested the efficacy of self-modulation of the dopaminergic midbrain with high-field 7-Tesla functional MRI biofeedback in a randomized, controlled, proof-of-principle trial that targeted motivation regulation. A total of N = 62 unmedicated participants (MDD and healthy controls) were randomized to receive either Active or Sham 7-Tesla functional MRI biofeedback and completed clinical assessments pre- and up to 30-days post-training. Factor analysis of clinical symptom change revealed a single latent clinical improvement factor that was significantly improved in the Active MDD compared to the Sham MDD group, immediately post-training (β = 15.85, t = 2.31, p = 0.03), and at 24-hours post-training (β = 22.84, t = 2.45, p = 0.02); effects were diminished and no longer significant at 7-day and 30-day follow-ups. Results of specific phenotypic clinical analysis revealed that depressed mood (F = 5.04, p = 0.029) and negative affect (F = 5.21, p = 0.027), but not positive affect, were most improved by the Active biofeedback intervention. Active biofeedback training engaged functional coupling over time between the VTA and the lateral frontal cortex in the MDD group (F = 6.03, p = 0.017), and greater overall VTA regulation was associated with clinical improvement (R = 0.268, p = 0.048). Together, these results indicate the potential utility of dopaminergic midbrain-based biofeedback training for improvement of mood and negative affect in MDD.

PMID 42763338
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