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CTC-111 (Anact C)

✓ Approved

Meiji Holdings · PROC

What is CTC-111?

CTC-111 is a therapeutic agent developed by Meiji Holdings. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesAnact C
CompanyMeiji Holdings
Molecular TargetPROC
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Mechanism of Action

Molecular Targets

CTC-111 acts on 1 molecular target:

PROCprotein C, inactivator of coagulation factors Va and VIIIa (APC, PROC1)
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Therapeutic Indications

CTC-111 is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved
Skin and subcutaneous tissue disordersPurpura fulminans✓ Approved

Related Research Articles

PubMedCancer treatment and research communications2026-09-19

Beyond Exons 19 and 21: mapping the clinical and molecular diversity of uncommon EGFR mutations in a Brazilian NSCLC cohort.

de Sousa Juliana Cordeiro JC, Nogueira Cleto C, Veloso Guilherme de Sousa GS, da Silva Emerson Lucena EL et al.

Uncommon and complex EGFR variants respond variably to tyrosine kinase inhibitors, and data on their frequency in Brazil are scarce. We retrospectively analysed 141 patients with EGFR-mutated lung adenocarcinoma at a single Northeastern Brazilian centre. All profiling used treatment-naive diagnostic specimens: next-generation sequencing (NGS) in 111 patients (78.7%) and rapid PCR or single-gene assay in 30 (21.3%). Concurrent alterations and PD-L1 were assessed where panels covered those genes. Overall survival was estimated by Kaplan-Meier analysis and log-rank test. Twenty patients (14.2%; 95% CI 8.9-21.1%) harboured an uncommon or complex variant, and detection depended on platform: 19 of 111 NGS-tested (17.1%) versus 1 of 30 hotspot-tested (3.3%). Exon 20 insertions predominated (8, 40%; five distinct variants), followed by exon 18 substitutions (5), compound genotypes (5) and other point mutations (2). T790M and C797S occurred de novo in two treatment-naive tumours with a classical driver. The subgroup was 85% female, median age 69.5 years. TP53 co-mutation was frequent and similar between groups (61.1% versus 58.2%; p = 1.00), whereas STK11 and KEAP1 were absent. Median overall survival was 1,375 days (95% CI 391 to not reached) with three deaths, and no difference from classical drivers was detected (p = 0.48), an underpowered result not establishing equivalence. Uncommon and complex EGFR variants accounted for 14.2% of EGFR-driven lung adenocarcinoma here, confirming previous Brazilian data with added molecular resolution. Detection was over four times as frequent with broad NGS as with hotspot testing, making comprehensive profiling prerequisite for genotype-directed treatment.

PubMedBMC cardiovascular disorders2026-09-19

Association of ACE2 gene polymorphisms with risk of pulmonary arterial hypertension in neonates with congenital heart disease.

Chen Youfang Y, Wang Cuiling C, Lin Qingfan Q, Chen Jin J et al.

Studies have confirmed a correlation between angiotensin-converting enzyme 2 (ACE2) gene polymorphisms and the risk of hypertension; however, its correlation with congenital heart disease (CHD)-related-pulmonary arterial hypertension (PAH) risk in neonates has not been reported. The study enrolled 321 Han Chinese neonates, comprising 113 healthy controls and 208 patients with left-to-right shunt CHD. Among the CHD patients, 98 cases were classified as the PAH subtype [CHD PAH (+)]. Tag SNP genotyping was performed using Sanger sequencing. Associations between three ACE2 SNPs (rs2074192, rs2285666, and rs2106809) and CHD PAH (+) neonates were assessed via sex-stratified logistic regression. Differences in circulating ACE2 and angiotensin1-7 [Ang(1-7)] levels across ACE2 haplotypes were compared using analysis of variance (ANOVA). No significant associations were observed between the three ACE2 SNPs and susceptibility to CHD or the risk of PAH in either univariable or multivariable analyses. In females, the CCT haplotype showed a nominally suggestive association with CHD-PAH in both the univariable model (OR = 0.216, 95% CI: 0.047-0.740; P = 0.025; FDR_P = 0.074) and the multivariable model (OR = 0.187, 95% CI: 0.039-0.670; P = 0.018; FDR_P = 0.053). A nominal difference in circulating Ang-(1-7) levels was also observed across haplotypes among females, with higher levels in CCT haplotype carriers than in those carrying the CTC or TCT haplotypes (160.16 ± 19.24 pg/mL vs. 140.54 ± 28.40 pg/mL and 139.77 ± 29.85 pg/mL, respectively; P = 0.037). However, this difference did not survive FDR correction (FDR_P = 0.074). Our study showed that there was no significant association between ACE2 SNPs or haplotypes and the risk of CHD-PAH in neonates. Our study is an observational study. According to the International Committee of Medical Journal Editors (ICMJE), purely observational studies (in which the allocation of medical interventions is not under the investigator's discretion) do not require registration.

PubMedAngewandte Chemie (International ed. in English)2026-09-19

Superoxide-Anion-Dominated Labeling of Graphene Defects in an Interfacial Nanoreactor of Electron-Donated Substrate.

Yang Qian Q, Yin Maoyun M, Jin Yan Y, Wang Rong R et al.

Harnessing the chemical reactivity of defects delivers a fundamental tool for precise nanoscale characterization of graphene defects. Herein, we develop a confined photochemical strategy based on the photosensitization of dye molecules targeted at the chemically active defects of graphene to label the defects. The graphene/copper interface enriches the electrons of graphene defects to construct a nanoreactor within defect-positioning interfaces, which modulates the preferential adsorption and the photosensitization reaction pathway of photoexcited methylene blue (MB). The nanoscale reactor preferentially channels the reaction through the Type I electron-transfer pathway, significantly triggering the •O2 - generation while concomitantly attenuating the competing Type II energy-transfer pathway. Subsequently, the •O2 - species deduce the selective etching reaction of Cu at defect sites, with the reaction kinetics following the Higuchi model. Moreover, the etching process exhibits pronounced crystallographic specificity, as evidenced by distinct pit morphologies and etching rates on the copper (111), (110), and (100) crystalline planes. DFT calculations confirm preferential adsorption and favorable electron transfer from defects to •O2 - species, unravelling the spatially confined nature of the etching reaction at graphene defects. Collectively, our results demonstrate how localized electronic states can dictate the interfacial reaction landscapes, advancing defect chemistry-guided identification/modification methodology of two-dimensional materials.

PubMedMolecular neurobiology2026-09-19

Identification and Validation of Candidate Biomarkers Co-expressed with Creatine Metabolism-Related Genes in Ischemic Stroke Based on Transcriptomics Data.

Li Jingjun J, Feng Xiaoxuan X, Liu Chang C, Song Yang Y et al.

Ischemic stroke (IS) is a major cause of death and disability, and creatine metabolism (CM) is potentially involved in its development. This study examined IS candidate biomarkers co-expressed with CM-related genes (CMRGs). IS data and CMRGs were sourced from public databases and published research. We identified candidate genes by intersecting genes from weighted co-expression network analysis and differential expression analysis. Candidate biomarkers were selected via machine learning. A diagnostic nomogram was constructed, and functional roles were explored via enrichment and immune infiltration analyses. Candidate biomarker expression was preliminarily validated by reverse transcription quantitative polymerase chain reaction in a small clinical cohort. Intersection analysis of the 336 differentially expressed genes and 3914 module genes yielded 111 candidate genes. Subsequently, F12 and PLXDC2 were identified as candidate biomarkers, and these genes were upregulated in IS samples. The nomogram based on these candidate biomarkers showed promising capacity for differentiating sample types in the training set, warranting further evaluation in independent cohorts. In addition to enrichment in pathways such as oxidative phosphorylation, VEGF-VEGFR2 signaling, and interleukin signaling, F12 and PLXDC2 were also strongly and positively correlated with neutrophils (r > 0.30, P < 0.001). Further screening highlighted cyclosporin A and trichostatin A as drugs that could simultaneously target both candidate biomarkers. This study identified F12 and PLXDC2 as candidate biomarkers co-expressed with CMRGs, offering preliminary insights that warrant further investigation in larger cohorts.

PubMedAnales de pediatria2026-09-19

Learning how to activate the chain of survival at school: Impact of an innovative educational intervention in children aged 5 to 8 years.

García-Martínez María M, Martínez-Isasi Santiago S, Varela-Casal Cristina C, Rodríguez-Núñez Antonio A

To improve the prognosis of cardiac arrest, annual school-based first aid training is recommended from an early age. However, there is limited scientific evidence supporting specific pedagogical strategies for this purpose. This study evaluated the impact of interactive teaching resources compared with traditional instruction on the acquisition and retention of skills related to activating the chain of survival in schoolchildren aged 5-8 years. We conducted a quasi-experimental study was conducted in five schools. A total of 298 schoolchildren were included: 111 in the control group (traditional instruction) and 187 in the intervention group (learning with a "never-ending book" and a telephone simulator). Assessments were carried out immediately after training (E0) and at 12 months (E1) using a simulation scenario and a checklist. In the initial assessment (E0), the intervention group achieved superior results in four key variables. At the 12-month evaluation (E1), the intervention group maintained significant advantages in competencies related to activating emergency medical services and effective communication with the dispatcher. The ability to use the phone in hands-free mode declined over time in both groups, while the ability to recall a parental phone number improved. Simple hands-on and interactive resources can improve both the acquisition and retention of basic skills required to activate the chain of survival. Their implementation in schools is feasible, cost-effective, and promotes practical learning from an early age.

PubMedResuscitation plus2026-09-19

Accuracy of ventilation feedback devices compared with a reference standard during asynchronous ventilation with continuous chest compressions in a simulated cardiac arrest: a prospective non-randomized cross-over study.

Duchatelet Christophe C, Segher Kristof K, Tackaert Thomas T, Vanwulpen Maxim M et al.

This study aimed to evaluate the accuracy of two commercially available ventilation feedback devices (VFD) in measuring ventilation rate and tidal volume during simulated cardiopulmonary resuscitation (CPR) with continuous chest compressions and asynchronous ventilations in the presence of reversed airflow. Prospective, simulation-based, non-randomized cross-over study. Twenty emergency department nurse practitioners performed manual ventilation on an intubated high-fidelity manikin during two 1-minute trials (one per device), targeting 10 breaths/min during continuous chest compressions (100-120/min). Ventilation parameters displayed by EOLifeX® and AccuVent® were compared with measurements from a high-fidelity pneumotachograph (HFRP). Data is presented as mean (standard deviation, min-max range). CI = confidence interval. EOLifeX®: From HFRP flow data, 254 ventilations were identified (rate 12/min [1; 8-14], tidal volume 544 mL [32; 482-604]). All showed reversed airflow with an average of 49 mL [13; 19-72]. VFD displayed values overestimated ventilation rate and underestimated tidal volume (111/min [5; 99-121] and 104 mL [14; 68-240]; biases +99 breaths/min, 95% CI 96.6-101.4, and -440 mL, 95% CI -456.3 to -423.7). AccuVent®: From HFRP flow data, a total of 222 ventilations were identified (rate 12/min [1; 8-13], tidal volume 532 mL [35; 460-614]). All showed reversed airflow with an average of 56 mL [15; 22-78]. VFD displayed values were similar for rate (12/min [1; 8-13]) but underestimated tidal volume (360 mL [24; 292-398]; bias -172 mL, 95% CI -191.9 to -152.1). During simulated CPR with continuous compressions and asynchronous ventilations, VFDs demonstrated clinically relevant inaccuracies. Validation under realistic resuscitation conditions are needed.

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