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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

PubMedJournal of physics. Condensed matter : an Institute of Physics journal2026-07-25

Probing superexchange interaction in a very hard 3d-4f single-molecule magnet by inelastic neutron scattering.

Qu Shuixian S, Zhai Yuan-Qi YQ, Stewart Ross R, Liu Xinzhi X et al.

We report a combined experimental and theoretical investigation of the spin dynamics in the very hard 3d-4f single-molecule magnet {Cr 3 Dy 3 }, where a central fluorido bridge (µ 3 -F⁻) suppresses zerofield quantum tunneling of magnetization (QTM). Utilizing inelastic neutron scattering (INS), heat capacity (HC) and ac susceptibility techniques, we have probed the low-lying magnetic excitations and their response to applied magnetic fields in polycrystalline samples. Full ab initio calculations, incorporating the experimental data, have provided an unambiguous determination of the ferromagnetic Dy-Dy coupling (J Dy-Dy = 0.016 meV) mediated by the µ 3 -F⁻ bridge and antiferromagnetic Cr-Dy interactions (J Cr-Dy = -0.215 meV). The significant energy gap between the ferrimagnetic ground state and the lowest exchange-induced excited state (1.03 meV) provides a direct mechanistic basis for the suppression of QTM, leading to its exceptional single-molecule magnet property.

PMID 42497901
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PubMedFrontiers in immunology2026-07-25

A network meta-analysis of endocrine adverse events induced by immune checkpoint inhibitors in colorectal cancer.

Chen Boyu B, Liu Jing J, Gan Kexin K, Yang Liqun L et al.

Immune checkpoint inhibitor (ICI) therapy for colorectal cancer (CRC) can be accompanied by endocrine adverse events, yet the comparative risk across commonly used regimens remains unclear. We therefore conducted a network meta-analysis of randomized controlled trials in CRC published up to November 22, 2025, estimating risk ratios (RRs) with 95% confidence intervals (CIs) and assessing risk of bias. Six RCTs were included. Relative to conventional therapy, ICI-based regimens were associated with a higher thyroid-related toxicity burden. Pembrolizumab and ICI+tyrosine kinase inhibitor (TKI) significantly increased the risk of hypothyroidism, whereas hyperthyroidism was significantly higher with ICI+TKI and ICI plus chemotherapy plus an anti-angiogenic antibody (ICI+Chem+Antiangio-Ab). Grade 1-2 adverse events were consistently increased across ICI-based treatments. For thyroiditis, diabetes mellitus, adrenal insufficiency, and grade 3-4 adverse events, effect estimates were imprecise with wide 95% CIs; nevertheless, SUCRA rankings tended to place ICI+TKI toward the higher-risk end for thyroiditis and diabetes. These findings indicate that ICI-containing strategies in CRC increase risks of endocrine adverse events-particularly for thyroid dysfunction-supporting the need for proactive endocrine monitoring and standardized management, while highlighting the limited precision of current evidence for rarer endpoints and severe toxicity. https://www.crd.york.ac.uk/PROSPERO/view/CRD42023469312, identifier CRD42023469312.

PMID 42500681
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PubMedSmart molecules : open access2026-07-25

Endocytosis-independent cytosolic entry of messenger RNA via fluorous bilayer zippering attenuating Toll-like receptor signaling and enables ischemic tissue salvage.

Wang Yue Y, Xie Haitao H, Xiang Guoqing G, Li Yanhua Y et al.

A fundamental constraint of conventional messenger RNA (mRNA) delivery systems is their obligatory trafficking through endosomal-lysosomal compartments, wherein cargo degradation and activation of endosomal Toll-like receptors precipitate substantial translational attrition and deleterious inflammatory cascades. We herein report a chemically engineered platform that circumvents these limitations ab initio. Through strategic perfluoro-acylation of branched polyethyleneimine (PEI, 25 kDa) with pentafluoropropionic anhydride, we install approximately 26 fluoro-amide "zipper" moieties per polymer chain that orchestrate direct, energy-independent trans-bilayer translocation without recruitment of clathrin, caveolae, or lipid raft microdomains-thereby precluding lysosomal entrapment and catabolism. Bio-orthogonal copper-free click chemistry between azide- and dibenzocyclooctyne (DBCO)-terminated PEI-F derivatives, coupled with redox-labile disulfide crosslinkers, engenders polyplexes of exceptional extracellular stability that undergo quantitative glutathione-triggered disassembly within the cytosolic milieu. This endosome-evasive entry mechanism effectively sequesters single-stranded mRNA from Toll-like receptor 3, TLR7, and TLR8 surveillance, establishing a "TLR-attenuated" delivery paradigm characterized by undetectable interferon-α, interferon-β, TNF-α, and IL-6 induction. In human umbilical vein endothelial cells, GFP-mRNA transfection exceeds 90% fluorescent positivity with 4.8-fold superior luciferase expression relative to Lipofectamine™ 3000, whilst maintaining >95% viability. Therapeutic translatability is demonstrated in a murine hindlimb ischemia model, wherein a single 10 μg intramuscular dose of mVEGF-A polyplexes restores blood perfusion to 118% of baseline within 28 days-representing marked superiority over the commercial gold standard and effectuating complete tissue salvage without necrosis. Comprehensive hematological and immunological profiling corroborates the absence of hematotoxicity, systemic inflammation, or innate immune activation. This modular, purely synthetic platform resolves the classical stability-availability paradox whilst eliminating the immunogenic liabilities inherent to endocytic delivery, furnishing a readily translatable scaffold for precision regenerative medicine.

PMID 42500712
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PubMedToxicology2026-07-25

Deoxynivalenol Induces Macrophage Extracellular Trap Formation via the PER2-c-Myc-ROS Axis.

Zhao Baimei B, Tan Shiqing S, Li Junyao J, Nepovimova Eugenie E et al.

Deoxynivalenol (DON), a Fusarium-derived mycotoxin, disrupts immune homeostasis and induces immunotoxicity. Macrophage extracellular traps (METs) are key effectors in innate immunity and inflammation, yet whether DON triggers METs formation and the underlying mechanisms remain unclear. This study aims to investigate the molecular mechanism by which DON induces METs generation through circadian rhythm immune checkpoints involving the PER2-c-Myc axis. Using RAW264.7 and THP-1 macrophage models, we combined siRNA-mediated Per2 knockdown, and pharmacological inhibitors to dissect the mechanisms of DON-induced METosis. We showed that DON (2-4μM) triggered a biphasic METosis. The early phase (1-2h) represents vital or non-suicidal METosis, characterized by F-actin depolymerization, rapid DNA release, and acute extrusion of MET markers histone H4, H2AX, CitH3, and MPO, reflecting an acute defense response. The late phase (8-12h) corresponds to suicidal METosis, featuring a secondary surge in MET markers and typical reticular ultrastructures, indicating impaired repair and pathological progression. Mechanistically, DON co-activates an ROS-driven pathway and a PADI2-mediated histone modification pathway to drive suicidal METosis. PER2 acts as a circadian-immune checkpoint, positively regulating both pathways while suppressing c-Myc and maintaining its phosphorylation balance. In turn, c-Myc inhibits ROS signaling and MET release. Thus, DON-associated changes in PER2 expression, causing its aberrant upregulation, c-Myc suppression, and consequent derepression of ROS-driven METosis. This study elucidates a novel molecular mechanism by which DON promotes suicidal METosis in macrophages via the PER2-c-Myc-ROS signaling, providing new molecular targets for understanding DON-induced immunotoxicity.

PMID 42498174
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PubMedBioorganic chemistry2026-07-25

Oxadiazole and hydrazone derivatives of benzimidazothiazine as potential antifungal and anti-tubercular agents.

Pandikatte Nefisath N, Sudhakar Shashiprabha S, Vilas Gowda K B KB, Ramu Ramith R et al.

The current study focuses on the synthesis and pharmacological evaluation of novel oxadiazole and hydrazone derivatives of 4-oxo-4H-benzo[4,5]imidazo[2,1-b][1,3]thiazine-2-carbohydrazides (5a-f and 6a-f). The compounds were synthesised via a conventional reflux method and characterized using FT-IR, NMR (1H and 13C), and LC-MS techniques. Antifungal activity of all compounds was evaluated against Candida albicans using the broth microdilution method, and compounds 6b and 6 f showed greater inhibitory potential than the reference drug, Fluconazole. Biofilm inhibition assay, supported by SEM analysis, showed notable inhibitory effects, particularly for compounds 6b and 6 f, and strong suppression of hyphal development, as analyzed in the filament inhibition assay. In addition, biofilm gene expression was assessed by RT-PCR for the target compounds, demonstrating greater inhibitory effects on gene expression for 6b and 6 f than for Fluconazole. Furthermore, in silico studies identified compounds 6b and 6 f as potential lead candidates due to their multi-target interactions with Candida albicans virulence-associated proteins. The anti-tubercular activity was evaluated on Mycobacterium tuberculosis (H37Rv strain, ATCC No. 27294), in which the compound 5a from the oxadiazole series exhibited good anti-tubercular activity, and in the hydrazone series, the compound 6b exhibited excellent anti-tubercular activity.

PMID 42497767
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PubMedACS physical chemistry Au2026-07-25

Understanding Molecular Excited States at the Metal-Molecule Interface via Transition Density Matrix AnalysisA Case Study of Azobenzene Thiols on Gold.

Jahn Nicolas N, Titov Evgenii E

Noble metal nanoparticles are rapidly gaining popularity as novel catalytic platforms to influence chemical reactions in various ways. Despite an increasingly large number of studies, many key processes especially at the metal-molecule interface are fundamentally still not fully understood up to this day. Throughout this work, we present a systematic study targeting the molecular excited states of covalently linked azobenzenes (ABs) on gold via a combination of time-dependent density functional theory and tight-binding calculations with transition density matrix analysis. We find that the optically bright ππ* state is strongly resonant to close-lying local gold excitations, which leads to splitting and redshift of the ππ* state and increased UV/vis absorption around the ππ* excitation energy. We show that these findings hold true across different AB isomers and demonstrate how a systematic variation of the AB-gold distance leads to a gradual localization of the ππ* excitation. Moreover, we discuss how a direct electronic interaction between the AB and the gold surface leads to the formation of delocalized hybrid states and investigate the exciton formation of AB dimers at the metal interface. Our results are carefully verified across a wide range of computational parameters including a large number of different density functionals, basis sets, and gold clusters of varying forms and sizes. The presented workflow is easily applicable to other functional molecules on metal surfaces to further broaden the understanding of substrate-surface interactions at the interface.

PMID 42500224
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