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imatinib mesilate

✓ Approved

Dako · KIT · 辅助诊断

什么是 imatinib mesilate？

imatinib mesilate 是一种辅助诊断，由Dako研发。该药已获批，用于治疗相关适应症，给药途径：Others。

药物档案

公司Dako
药物类别辅助诊断
分子靶点KIT
给药途径Others
状态Approved
来源： ClinicalTrials.gov, Dako

作用机制

分子靶点

imatinib mesilate 作用于 1 个分子靶点：

KITKIT proto-oncogene, receptor tyrosine kinase (MASTC, CD117)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

imatinib mesilate 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancer✓ Approved

相关研究文献

PubMedCells2026-10-26

Stem Cell-Based Therapies in Companion Animals: Molecular Mechanisms, Clinical Applications, and Translational Perspectives.

Liu Weina W, Wang Yu Y, An Wei W, Wang Zhenlong Z et al.

Stem cell-based therapies, as regenerative and immunomodulatory strategies, show substantial potential in companion animals through tissue repair, functional recovery, and immune modulation. Despite advances in human stem cell research, veterinary clinical translation remains constrained by small sample sizes, short follow-up periods, and non-standardized cell dosing regimens and delivery protocols. The expanding repertoire of stem cell-based modalities and technologies-including mesenchymal stem cells, induced pluripotent stem cells, extracellular vesicles, and tissue engineering-provides promising avenues for clinical application. This review summarizes recent progress in stem cell-based therapies across multiple disease systems in dogs and cats, with particular attention to the molecular mechanisms underlying regenerative and immunomodulatory effects, cross-species translational strategies, current challenges, and combinatorial therapeutic approaches in companion animals. By examining mechanistic findings alongside preclinical and early clinical evidence, this review highlights the limitations of current knowledge and identifies research priorities for evaluating the safety and efficacy of stem cell-based therapies in dogs and cats.

PMID 42929856
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PubMedVeterinary medicine international2026-10-26

Zoonotic Potential of Non-Helicobacter pylori Helicobacter Species Associated With Dogs and Cats in Human Infections: A Systematic Review.

Al-Gburi Nagham Mohammed NM

Non-Helicobacter pylori Helicobacter (NHPH) spp. are clinically relevant organisms found in humans and several animal hosts. Dogs and cats are natural hosts of multiple gastric and enterohepatic NHPH spp. and may represent potential sources of human exposure. This systematic review aimed to synthesize the clinical, epidemiological, and molecular evidence concerning human infections involving dog- and cat-associated NHPH spp. and to evaluate the evidence for a possible epidemiological association with companion animals. PubMed and Scopus databases were searched for studies published from 2000 through the final search on April 15, 2026. Eligible studies reported human infection with NHPH spp. involving H. heilmannii sensu stricto (s.s), H. felis, H. bizzozeronii, H. salomonis, or H. canis. The following information was extracted: study and patient characteristics, NHPH species, human samples, diagnostic techniques, molecular confirmation, immunological state, clinical results, and exposure to dogs and/or cats. The risk of bias was evaluated using the Joanna Briggs Institute (JBI) critical appraisal checklist appropriate for each study design. Of 350 records identified, 51 studies met the inclusion criteria. The evidence consisted predominantly of case reports. H. heilmannii-related organisms were the most frequently reported, followed by H. canis, H. felis, H. bizzozeronii, and H. salomonis. Gastric NHPH infections were predominantly associated with gastric disease, while H. canis was mainly associated with systemic and extragastric infections, especially in immunocompromised or clinically vulnerable patients. Molecular confirmation was reported in 66.7% of studies (34/51), with one additional study providing molecular confirmation for only 2 of 22 cases. Dog and/or cat exposure was documented in 41.2% of studies (21/51). Although several studies identified the same NHPH spp. in humans and companion animals, paired strain-level molecular evidence remained limited and was insufficient to establish the direction of transmission. Numerous gastrointestinal and systemic infections in humans have been linked to NHPH spp. found in dogs and cats. According to available data, dogs and cats may act as reservoirs or sources of human NHPH infection, given the recognized zoonotic potential of these pathogens. However, direct animal-to-human transmission and its direction have not been conclusively established. This is largely due to the limited availability of strain-level molecular comparisons and paired human-animal sampling. To clarify transmission routes and improve integrated One Health surveillance, consistent molecular identification and comparative genomic studies are therefore required.

PMID 42928729
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PubMedBiosensors2026-10-26

Development of a One-Pot MIRA-CRISPR/Cas12b Fluorescence Biosensing Platform for Rapid Detection of Brucella canis.

Huo Suxin S, Zhu Yinchu Y, Ji Congyun C, Fan Fu F et al.

Brucellosis is an important zoonotic disease worldwide, and Brucella canis (B. canis) is an emerging concern in companion animal health. Rapid and reliable detection of B. canis in dogs is essential for disease control. Herein, we developed a one-pot MIRA CRISPR/Cas12b fluorescence biosensing platform targeting the conserved omp31 gene. The platform integrates MIRA mediated isothermal amplification with CRISPR/Cas12b-based target recognition and collateral cleavage. After optimization, the assay achieved a detection limit of 5 copies/reaction within 20 min, comparable to qPCR. No cross reactivity was observed with seven common canine pathogens. Among 128 clinical blood samples, the biosensor showed complete agreement with qPCR, achieving 100% sensitivity and 100% specificity. These findings demonstrate that the biosensor provides a rapid, sensitive, and specific approach for B. canis detection, with potential for decentralized veterinary testing through its endpoint visual fluorescence readout and applications in One Health surveillance.

PMID 42930125
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PubMedAnnals of hematology2026-10-26

Sequential emergence of FLT3-ITD and BCR::ABL1 during disease progression in relapsed acute myeloid leukemia.

Irifune Hidetoshi H, Semba Yuichiro Y, Uehara Yasufumi Y, Ohta Takanori T et al.

Emergence of BCR::ABL1 during FMS-like tyrosine kinase 3 (FLT3) inhibitor therapy is a rare resistance mechanism in acute myeloid leukemia (AML). We report a case of relapsed AML with sequential clonal evolution after allogeneic hematopoietic stem cell transplantation (allo-HSCT). A previously healthy man in his 30s was diagnosed with AML with maturation; initial cytogenetics were normal, and both FLT3-internal tandem duplication (FLT3-ITD) and BCR::ABL1 were absent, while targeted sequencing identified an FBXW7 mutation. After induction failure, he underwent allo-HSCT. At post-transplant relapse during venetoclax plus azacitidine maintenance, FLT3-ITD and WT1 mutations newly emerged. Quizartinib induced remission, but a second relapse occurred with emergence of BCR::ABL1 while FLT3-ITD persisted. Cytogenetics showed t(9;22)(q34;q11), and FISH confirmed BCR::ABL1 fusion in 73% of bone marrow cells, with the minor transcript (p190) confirmed by quantitative PCR. Despite no ABL1 kinase domain mutations, imatinib and ponatinib failed to control the disease. These findings suggest that BCR::ABL1 emergence may represent a bypass resistance mechanism arising under quizartinib-associated selective pressure.

PMID 42928344
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PubMedJournal of sleep research2026-10-26

Sleep Duration Phenotypes and Dynamic Homeostasis: A Wave-Model Framework.

Zhdanova Irina V IV, Kharchenko Vasili V, Barbato Giuseppe G, Wehr Thomas A TA

Are sleep duration and sleep intensity manifestations of the same phenotype, or are they distinct, complementary traits? We addressed this question by removing two major constraints on phenotype expression: limited sleep opportunity and prior sleep deficit. Across 105 baseline 8-h nights and 420 extended 14-h nights in 15 individuals, sleep duration and NREM intensity behaved as two largely independent traits. Baseline expression of each parameter predicted its own subsequent expression during chronic sleep abundance but failed to predict the companion trait either within or between conditions. We then evaluated external evidence from chronic 4- and 6-h sleep restriction alongside extreme natural sleep-duration phenotypes, interpreting these findings through the wave model of sleep dynamics. In this framework, sleep duration reflects the geometry of sleep-cycle oscillations, determined primarily by the width of the sleep-state stability landscape (formally represented as a Morse potential well). Conversely, NREM intensity reflects oscillation amplitude, providing a visible signature of deviation from homeostatic equilibrium. While acute perturbation alters amplitude, chronic perturbation induces adaptive changes in landscape width, preserving a characteristic deviation from equilibrium despite severe shifts in underlying state instability and allostatic strain.

PMID 42928455
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PubMedJournal of evaluation in clinical practice2026-10-26

Restoring Diagnostic Stability in Complex Illness: Integrated Longitudinal Feedback in Clinical Care (RD).

Hirschman Shayle I SI

Modern healthcare produces persistent diagnostic instability in complex illness despite expanding technological capability and clinical specialization. Prior work identified structural diagnostic failure (SDF), a systemic condition where diagnostic responsibility fragments across encounters and specialties, blocking the continuous integration of clinical information across time. Under these conditions, clinical care persists-tests are ordered, referrals occur, and treatments are attempted-yet diagnostic state estimation stalls, producing repeated action without explanatory convergence. This article examines the operational structures required to restore diagnostic stability. The proposed solution centres on restoring protected longitudinal diagnostic responsibility through two integrative clinical roles: the Doctor of Clinical Diagnostics (DCD) and the Nurse Practitioner of Clinical Diagnostics (NPCD). Clinicians in these roles are trained to synthesize evolving clinical evidence across encounters, organ systems, and specialties. They function not as replacements for specialty diagnosis but as longitudinal integrators responsible for maintaining diagnostic continuity when illness spans domains or lacks clear specialty ownership. Within this architecture, diagnostic reasoning is preserved through integrated longitudinal feedback (ILF), a structural mechanism that maintains continuity of diagnostic information across encounters. This allows new findings, treatment responses, and patient experience to refine diagnostic understanding rather than resetting interpretation. Together, these mechanisms convert episodic encounter-based care into a closed-loop diagnostic system capable of achieving explanatory convergence in high-variance clinical environments. The framework generates empirically testable predictions in clinical environments characterized by multisystem comorbidity and diagnostic instability. This provides a pathway for evaluating whether restoration of longitudinal diagnostic responsibility improves diagnostic convergence, reduces redundant evaluation, and stabilizes care for complex illness.

PMID 42929722
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