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Last update 08 May 2025

CRAF x Cytokines

Last update 08 May 2025

Basic Info

Related Targets

CRAFCytokines

Drugs associated with CRAF x Cytokines

Semapimod Mesylate

Target

CRAF x Cytokines

Mechanism

CRAF inhibitors [+2]

Active Org.-

Originator Org.

Ferring BV

Active Indication-

Inactive Indication

Chemotherapy-induced damage [+5]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with CRAF x Cytokines

NCT00741910

/ CompletedPhase 2

Extension Study of CNI-1493 for Treatment of Moderate to Severe Crohn's Disease

Study CNI-1493-CD06 is an open, single-arm extension studies to CD03 and CD05. CDAI is the only efficacy measure assessed in this study. The safety of multiple courses of semapimod is to be determined by the incidence of clinical and laboratory adverse events.

Start Date01 Jul 2003

Sponsor / Collaborator

Ferring Pharmaceuticals A/S

NCT00740103

/ CompletedPhase 2

Long-term Study of Semapimod (CNI-1493) for Treatment of Moderate to Severe Crohn's Disease With Reference to Study CNI-1493-CD-04, 1 or 3 Days' Treatment vs. Placebo

CNI-1493-CD05 is an open-label extension study of CNI-1493-CD04. In the CD05 study, patients are eligible for up to 5 courses of semapimod 60 mg IV x 3 days every 6 - 8 weeks. Primary objective is assessment of the efficacy of cumulative doses of semapimod measured by decrease in Crohn's Disease Activity Index (CDAI).

Start Date01 Dec 2002

Sponsor / Collaborator

Ferring Pharmaceuticals A/S

NCT00739986

/ CompletedPhase 2

A Randomized, Double-Blind, Placebo-controlled Study of CNI-1493 for Treatment of Moderate to Severe Crohn's Disease 1 or 3 Days' Treatment vs. Placebo

Assessment of the number of days' treatment with semapimod necessary for efficacy, as measured by response rate to CNI-1493 as compared to placebo, in patients with moderate to severe Crohn's disease (CD).

Start Date01 Oct 2002

Sponsor / Collaborator

Ferring Pharmaceuticals A/S

100 Clinical Results associated with CRAF x Cytokines

100 Translational Medicine associated with CRAF x Cytokines

0 Patents (Medical) associated with CRAF x Cytokines

681

Literatures (Medical) associated with CRAF x Cytokines

01 May 2025·Research in Veterinary Science

Immunometabolic effects of β-glucan-trained immunity in newborn goats

Article

Author: Angulo, Miriam ; Angulo, Carlos

Debaryomyces hansenii CBS 8339 β-glucans induced trained immunity in newborn goats. However, the metabolic shifts and potential signaling pathways have not been described yet. Thus, the present study aims to prove, firstly, modifications in cell metabolism related to trained immunity induction (β-glucans) and inhibition (MCC950) in an in vitro model upon lipopolysaccharide (LPS) re-stimulation; secondly, metabolic changes and possible signaling pathways are related to immune memory induced by β-glucan per os in newborns after ex vivo re-stimulation with a bacterial pathogen. Immune training leads to augmenting glycolysis (glucose and lactate) metabolites. Nevertheless, these changes were unaffected by a NOD-like receptor (NLRP3) inhibitor. In vivo training with oral β-glucan doses also evidenced an increase in glycolysis metabolites mediated by up-regulating AKT/MTOR/HIF1Α genes signaling pathway in monocytes; β-glucan in vivo training up-regulated Dectin1, TLR4, TLR6 RAF1, IL1Β and IL6 gene expressions in monocytes, while TNFΑ gene down-regulated. In conclusion, the results demonstrated that D. hansenii β-glucan induced trained immunity in newborn goat monocytes after LPS re-stimulation through glycolysis shifts, which were not reverted by the MCC950 inhibitor.

01 May 2025·Phytomedicine

Qi-Huang decoction alleviates DSS-induced colitis with Candida albicans dysbiosis by enhancing innate immune response through Dectin-1-associated signaling

Article

Author: Zhu, Hanyu ; Liu, Chengcheng ; Shao, Jing ; Wang, Tianming ; Wu, Daqiang ; Luo, Qinai ; Wang, Zixu ; Wang, Changzhong ; Hu, Min ; Yang, Liu

BACKGROUNDUlcerative colitis (UC) is a chronic inflammatory disease of the gastrointestinal tract. Candida albicans, a common commensal fungus in the human gut, has been increasingly implicated in UC pathogenesis. Qi-Huang decoction (QHD), a traditional Chinese herbal formula known for its spleen-invigorating and purgative properties, is commonly used to restore gastrointestinal function.PURPOSEThis study investigates the therapeutic potential of QHD in treating colitis exacerbated by C. albicans and explores the underlying mechanisms of action.METHODSA mouse model of colitis was induced using dextran sulfate sodium combined with gavage of C. albicans. Following QHD treatment, colitis severity was evaluated by measuring survival rate, body weight, disease activity index, colon length, and fungal burden, and through histopathological analysis using hematoxylin-eosin staining. The expression of proinflammatory genes IL-1β and TNF-α was quantified, alongside protein levels of key molecules involved in Dectin-1 signaling, including Syk, CARD-9, NLRP-3, Raf-1, and NF-κB. Barrier integrity markers, such as Occludin and Claudin-1, were also examined. To further elucidate QHD's mechanisms, Dectin-1 was inhibited using laminarin. In vitro experiments assessed QHD's antifungal activity against three Candida strains through microdilution, spot assays, and time-kill tests. RAW 264.7 macrophages were employed to study the exposure of fungal cell wall β-glucan and subsequent phagocytosis. Molecular docking simulations predicted interactions between QHD's active compounds and the Dectin-1 receptor.RESULTSQHD significantly mitigated colitis severity and reduced fungal burden in vivo. QHD enhanced β-glucan exposure on the fungal cell wall, thereby stimulating phagocytosis by RAW264.7 macrophages. QHD effectively activated Dectin-1-mediated signaling pathways and increased proinflammatory levels in RAW 264.7 cells. In colitis mice, QHD treatment markedly reduced inflammation and Dectin-1 signaling following fungal clearance. However, Dectin-1 inhibition with LAM neutralized QHD's therapeutic effects, highlighting the pathway's importance in mediating QHD's efficacy. Interestingly, QHD alone elevated Dectin-1, NF-κB, TGF-β, and IL-10 levels, whereas reduced IL-1β and TNF-α expression, suggesting a dual modulatory role in inflammation. Molecular docking confirmed a potential direct interaction between QHD's bioactive components and the Dectin-1 receptor.CONCLUSIONQHD demonstrates promising therapeutic potential for managing Candida colitis by modulating immune responses and targeting Dectin-1 signaling pathways in clinical settings.

01 Apr 2025·Cytotechnology

Mechanism underlying the role of the circRNA OMA1/miR-654-3p/RAF1 axis in children with inflammatory bowel disease

Article

Author: Xu, Yufen ; Wang, Zhenhui ; Wu, Meirong ; Zhang, Ping

Inflammatory bowel disease (IBD), a chronic gastrointestinal disorder, often emerges during childhood and poses significant challenges due to its adverse effects on growth, development, and psychosocial well-being. Circular RNAs (circRNAs) have been implicated in the pathogenesis of diverse diseases. However, the specific biological role and mechanisms of circRNA OMA1 in children with IBD remain largely unexplored. This study investigates the functions and mechanistic pathways of circRNA OMA1 in the progression of IBD. Quantitative real-time PCR (qRT-PCR) was employed to quantify circRNA OMA1 and miR-654-3p expression levels in the serum of children with IBD and in HT-29 cells. Downstream miRNA and mRNA targets of circRNA OMA1 were predicted using StarBase and validated via luciferase reporter assays. An in vitro IBD model was established by treating the human colonic epithelial cell line (HT-29) with 2% dextran sulfate sodium (DSS). Cell viability and apoptosis were assessed using the MTT assay and flow cytometry, respectively. Expression of the apoptosis-related protein cleaved caspase-3 was analyzed via western blotting, and proinflammatory cytokine levels (TNF-α, IL-1β, and IL-6) were measured using ELISA. The expression of circRNA OMA1 was notably lower in the serum of children with IBD and in DSS-treated HT-29 cells than in healthy controls, whereas miR-654-3p expression was upregulated. Bioinformatics analyses revealed a direct interaction between circRNA OMA1 and miR-654-3p. Overexpression of circRNA OMA1 through plasmid transfection increased circRNA OMA1 levels and suppressed miR-654-3p expression in HT-29 cells under both basal and DSS-stimulated conditions. Conversely, transfection with a miR-654-3p mimic reversed these effects. Upregulation of circRNA OMA1 ameliorated DSS-induced injury in HT-29 cells by enhancing cell viability, reducing apoptosis, and downregulating cleaved caspase-3 expression. Moreover, circRNA OMA1 overexpression inhibited the secretion of inflammatory cytokines TNF-α, IL-1β, and IL-6. However, these protective effects were partially reversed by treatment with the miR-654-3p mimic. Additionally, miR-654-3p was shown to directly target RAF1, negatively regulating its expression. The proliferation-promoting and apoptosis-suppressing effects of miR-654-3p inhibitor treatment were mitigated by RAF1-siRNA. Conclusion: Upregulation of circRNA OMA1 alleviates DSS-induced colonic cell apoptosis and inflammation by modulating the miR-654-3p/RAF1 axis. These findings suggest that circRNA OMA1 could be a promising biomarker for the diagnosis and treatment of IBD.Supplementary InformationThe online version contains supplementary material available at 10.1007/s10616-025-00703-z.

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