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botulinum toxin type A (Coretox)

✓ Approved

Medytox · 治疗药物

什么是 botulinum toxin type A？

botulinum toxin type A 是一种治疗药物，由Medytox研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。

药物档案

商品名Coretox
公司Medytox
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, Medytox

治疗适应症

botulinum toxin type A 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Skin and subcutaneous tissue disordersSkin wrinkling✓ Approved
Musculoskeletal and connective tissue disordersMuscle spasmsPhase III

相关研究文献

PubMedBMC biology2026-10-26

A developmental shift in venom toxin expression underpins a major prey switch in Australian brown snakes.

van Thiel Jory J, Smith Cara F CF, Kazandjian Taline D TD, Patel Rohit N RN et al.

Many animals change traits over the course of their life history. It has been proposed that some of these developmental changes evolve in concert with shifts in ecology, but there are relatively few clear examples, and identifying the underlying molecular changes is challenging. Australian brown snakes (Pseudonaja spp.), one of Australia's most venomous snakes, may provide such an example, as previous work has shown that these species undergo a dietary shift from reptiles to mammals, accompanied by differences in venom activity. We show that the venom composition of adult brown snakes is distinguished by the collective expression of four procoagulant toxin families, which are absent in juvenile life stages, where venom composition is instead dominated by neurotoxins. The developmental onset of expression across all four procoagulant toxins correlates with a functional shift in venom activity to one that disrupts the blood-clotting system of mammalian prey. We further show that this developmental timing in both toxin expression and procoagulant venom activity coincides with a broader ecological transition in which Australian brown snakes begin to prey on mammals. In contrast, we found that the smallest brown snake species, a lizard specialist throughout its lifetime, only expresses neurotoxins and shows no comparable developmental shift in either procoagulant toxin expression or procoagulant activity. Our findings suggest that a coordinated shift in the expression of four procoagulant toxin gene families transitions the venom from a neurotoxic phenotype in lizard-feeding juveniles to a potent procoagulant phenotype in mammal-feeding adults. These results provide a clear example of how the concerted upregulation of multiple genes can drive a functional shift in a key ecological trait, linking changes in toxin gene expression to venom activity and, ultimately, to prey-capture strategy.

PMID 42928320
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PubMedIranian journal of biotechnology2026-10-26

Design and In Silico Evaluation of a Cry1Ac/XptC Hybrid Protein Targeting the APN Receptor in Manduca sexta.

Rashidabadi Mohammad Javad MJ, Solouki Mahmood M, Haddad-Mashadrizeh Aliakbar A, Emamjomeh Abbasali A et al.

The widespread use of Bacillus thuringiensis (Bt) Cry toxins has led to the evolution of resistance in target insect pests, posing a significant threat to sustainable agriculture. Manduca sexta, a major pest of Solanaceae crops, is developing resistance to conventional Cry1Ac toxins, necessitating the development of novel, high-efficacy molecular alternatives. This study aimed to design and computationally evaluate a novel hybrid toxin, RCGX1, by fusing functional domains of Cry1Ac and XptC proteins. The novelty of this approach lies in the rational fusion of domains from distinct bacterial toxin classes (Bacillus and Xenorhabdus) to create an emergent, neo-binding site, a strategy that moves beyond conventional single-toxin modifications. Functional domains were identified using InterPro: the galactose-binding domain of Cry1Ac (residues 462-609) and the SpvB toxin domain of XptC (residues 32-278). These domains were fused via a flexible (SSGG)4 linker to create the hybrid protein RCGX1. The 3D structure was predicted using I-TASSER and refined through energy minimization(converging in 730 steps). The quality of the model was validated using VERIFY3D, PROCHECK, and ERRAT. Molecular dynamics (MD) simulations (200 ns) were performed using GROMACS (CHARRM 27 force field) to assess structural stability. with analyses of Root Mean Square Deviation (RMSD), Root Mean Square Fluctuation (RMSF), Radius of Gyration (Rg), and hydrogen bond formation. Molecular docking by APN receptor was done using ClusPro to evaluate binding affinity and interaction sites. MD simulations demonstrated robust structural stability, with RMSD stabilizing at ~0.65 nm and Rg averaging 2.4 nm, indicating a compact and stable conformation. Docking revealed a high-affinity interaction (-1437.0 kcal.mol-1) unexpectedly mediated by the XptC moiety. The interface is anchored by a multivalent Arg36-Glu195 salt bridge, which is structurally reinforced by a local hydrophobic cage (Trp31/Phe34) and a specific hydrogen-bond network orchestrated by Gln125 and Gly284, creating a robust, engineered epitope distinct from canonical Cry toxins. The designed hybrid protein RCGX1 exhibits exceptional structural stability and a potent, specific binding affinity in silico. These results strongly suggest that RCGX1 is a compelling candidate for a new class of dual-function toxins. RCGX1 is thus positioned as a powerful lead candidate for experimental validation, offering a promising strategy capable of countering established Bt resistance pathways and paving the way for the development of next-generation biopesticides.

PMID 42928841
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PubMedDrug design, development and therapy2026-10-26

Traditional Chinese Medicine for Diabetic Kidney Disease: Predominantly Preclinical Evidence, Mechanistic Pathways, and Translational Challenges.

Zhang Jiani J, Lei Chaoqi C, Li Wei W, Jiang Yaqin Y et al.

Diabetic kidney disease (DKD) is a type of kidney microvascular complication resulting from diabetes, and it is one of the leading causes of end-stage kidney disease (ESKD). Existing drugs improve kidney function but do not markedly delay progression to ESKD or reduce mortality, so complementary approaches are urgently needed. This paper summarizes the evidence for traditional Chinese medicine (TCM) in DKD, organized by pathological mechanism. The studies identified here were almost exclusively preclinical, based on rodent models of DKD and on kidney cells exposed to high glucose. Across these studies, TCM interventions improved kidney function indices and attenuated glomerular and tubulointerstitial injury. The evidence is unevenly developed and was graded accordingly. Attenuation of oxidative stress, inflammation and kidney fibrosis is the best supported, whereas the modulation of autophagy, ferroptosis and the gut microbiota rests on a smaller number of studies. Podocyte injury, pyroptosis, apoptosis and mitochondrial dysfunction are each supported by only a few reports, and all of these mechanisms remain exploratory. Reported effects included restored antioxidant enzyme activity, reduced pro-inflammatory cytokine production, suppressed profibrotic signaling, increased levels of autophagy-related proteins, preserved glutathione peroxidase 4, reduced abundance of uremic toxin-producing gut taxa and preserved podocyte markers. Only a few agents have entered controlled trials, and some support comes from population-based cohorts, which report lower risks of ESKD and all-cause mortality among TCM users. Because reported outcomes are largely surrogate endpoints, TCM may currently be positioned only as a complementary or adjunctive therapy, pending confirmation in large multicenter randomized trials with hard kidney outcomes.

PMID 42928891
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PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-10-26

Persistent Pelvic Adhesions and Fibrotic Remodeling Following Ectopic Lesion Ablation in a Mouse Model of Endometriosis.

Yun Sohyeon S, So Kyeong A KA, Jeong Eunhee M EM, Hoover Marissa G MG et al.

Endometriosis is a chronic, estrogen-dependent inflammatory disorder characterized by ectopic endometrial-like lesions, fibrosis, and persistent pelvic pain. Although ectopic lesions are important contributors to pain, symptom severity often correlates poorly with lesion burden, suggesting lesion-independent mechanisms. Here, we investigated the contribution of ectopic lesion-derived cells to persistent pelvic adhesions, fibrotic remodeling, and endometriosis-associated behavioral alterations using a mouse model. A syngeneic model combined with inducible diphtheria toxin receptor (iDTR)-mediated cell ablation was used to selectively eliminate donor-derived progesterone receptor-expressing ectopic cells. Endometriosis was induced by transplantation of uterine tissue from Pgrcre/+Rosa26iDTR/mTmG donor mice into recipients, followed by diphtheria toxin-mediated lesion ablation. Lesion burden, pelvic adhesions, and fibrotic remodeling were assessed by imaging, histology, and molecular analyses, while behavioral outcomes were evaluated using non-evoked assays. Selective ablation eliminated detectable GFP-positive ectopic lesions. Histological and molecular analyses demonstrated significantly reduced collagen deposition and α-SMA-positive fibrotic remodeling within adhesion-associated tissues relative to established ectopic lesions, although these measures remained elevated above sham controls. However, despite lesion ablation, no statistically significant differences were detected between DT- and vehicle-treated mice in nesting or marble-burying performance, although the modest cohort size may have limited detection of partial behavioral effects. These findings indicate that, although fibrosis in adhesion-associated tissues was reduced relative to established ectopic lesions, residual fibrotic remodeling persisted above sham levels, whereas behavioral outcomes showed variable responses without a significant, uniform reversal, highlighting the potential importance of targeting fibrotic and adhesive remodeling in addition to ectopic lesions.

PMID 42929462
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PubMedFrontiers in molecular biosciences2026-10-26

When absence becomes functional: lysine deserts in protein regulation and evolution.

Szulc Natalia A NA

Lysine deserts-extended, continuous protein regions containing no lysine residues-occur across diverse proteomes, yet their definition, evolutionary origins and biological significance remain incompletely understood. In this Review, I examine the evidence linking local lysine depletion to protein regulation, with particular emphasis on ubiquitin- and proteasome-dependent pathways. Studies of toxin catalytic subunits and endogenous components of the ubiquitin-proteasome system show that introducing lysines at selected positions can alter ubiquitylation, protein turnover or function. These findings support a context-dependent model in which lysine deserts can limit the availability of ubiquitin acceptor sites within particular structural and enzymatic environments, rather than generally protecting entire proteins from modification or degradation. I discuss how lysine position, solvent accessibility, E3 ligase geometry and protein conformation determine the consequences of lysine introduction, and how N-terminal or non-lysine ubiquitylation as well as ubiquitin-independent proteolysis can bypass lysine depletion. I also consider the reported enrichment of lysine deserts in selected Actinobacteria and Mycobacterium phages, highlighting a testable Pup-proteasome adaptation hypothesis. Finally, I discuss potential functions beyond ubiquitylation and the methodological challenges of distinguishing selected lysine depletion from compositional bias or chance.

PMID 42928854
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PubMedCureus2026-10-26

Accidental Castor Bean (Ricinus communis) Poisoning in a Pediatric Patient: A Case Report and Literature Review.

Pineda Pulla Janeth J, Simaluisa Sambachi Sofia S, Allauca Barriga Danny D, Salguero Castellanos Diana D et al.

Castor bean (Ricinus communis) poisoning is an uncommon but potentially life-threatening toxicological emergency, particularly in children. No specific antidote exists, and treatment remains primarily supportive. We report the case of an 11-year-old previously healthy girl who accidentally ingested five chewed castor beans and developed repeated vomiting, diarrhea, abdominal pain, somnolence, and transient temporal disorientation. On admission, she was mildly dehydrated and exhibited transient neurological impairment accompanied by leukocytosis with neutrophilia, while hepatic, renal, and pancreatic function remained within normal limits. She was managed with supportive care, including intravenous fluids, antiemetic therapy, supplemental oxygen, serial laboratory testing, blood gas analyses, and continuous electrocardiographic monitoring. Gastrointestinal and neurological symptoms resolved within 48 hours, serial laboratory studies remained unremarkable, and no evidence of cardiac abnormalities or multiorgan dysfunction was observed during 72 hours of inpatient monitoring. This case highlights the considerable variability in the clinical expression of ricin toxicity and shows that complete recovery may occur despite ingesting multiple chewed castor beans, which theoretically increases toxin bioavailability. Early recognition, careful clinical observation, and timely supportive management remain the cornerstones of treatment until better prognostic markers become available.

PMID 42928937
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