北京若生智能科技有限公司
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AM

AM-87 (Difur)

✓ Approved

Cantabria Labs · LTB4R

什么是 AM-87？

AM-87 是一种治疗药物，由Cantabria Labs研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Difur
公司Cantabria Labs
分子靶点LTB4R, IL6R
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Cantabria Labs

作用机制

分子靶点

AM-87 作用于 2 个分子靶点：

LTB4Rleukotriene B4 receptor (GPR16, P2Y7)
IL6Rinterleukin 6 receptor (IL6RQ, IL-6R-1)
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

AM-87 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
Skin and subcutaneous tissue disordersPsoriasis✓ Approved

相关研究文献

PubMedNature communications2026-10-26

Systematic comparison of phenome-wide admixture mapping and genome-wide association at biobank-scale.

Cullina Sinead S, Shemirani Ruhollah R, Shi Zhuozheng Z, Mandla Ravi R et al.

Opportunities remain to leverage population structure in large scale genomic studies for additional insight. Admixture mapping (AM) identifies loci where disease risk differs by ancestral background, offering a complementary strategy to genome-wide association studies (GWAS) in admixed populations. We performed a systematic comparison of AM and GWAS across over 800 clinical phenotypes in Hispanic/Latino (HL) and African American (AA) participants from the BioMe biobank. We developed a well-calibrated AM pipeline tailored to the local ancestry structure of HL (N = 14,876) and AA (N = 8,819). While GWAS identified a greater number of significant associations, AM revealed 77 signals, including 48 not detected by GWAS. AM-tagged variants had higher minor allele frequency and population differentiation (Fst), while GWAS demonstrated higher odds ratios, underscoring the distinct genetic architecture identified by each method. This study emphasizes the importance of applying both GWAS and AM approaches to uncover previously unreported loci in admixed populations.

PMID 42928239
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PubMedAdvanced materials (Deerfield Beach, Fla.)2026-10-26

A Glycan Key Unlocks Microglia Targeting and Reprogramming to Promote Functional Recovery After Spinal Cord Injury.

Liu Ting T, Du Liangchao L, Ma Wanrong W, Long Ge G et al.

Spinal cord injury (SCI) triggers uncontrolled neuroinflammation driven by dysfunctional microglia and pro-inflammatory-biased reprogramming, yet precise therapeutic strategies remain limited. Here, we report a novel glycan-targeted nanoparticle system (ICT@APD) designed to enhance the microglia-reprogramming potential of icaritin (ICT) while overcoming its inherent narrow therapeutic window. By functionalizing nanoparticles with 2,5-anhydro-D-mannitol (2,5-AM), a high-affinity ligand for the microglia-specific transporter GLUT5, ICT@APD achieves selective microglial uptake and amplifies the capacity of ICT to reprogram microglia toward an anti-inflammatory phenotype. The targeted reprogramming consequently creates a positive microenvironment that promotes axon regeneration, neuronal survival, and synaptic reconstruction, leading to significantly improved locomotor recovery after SCI. Our findings establish a novel glycan-mediated microglial targeting and reprogramming strategy for SCI repair, which may extend to other central nervous system disorders and provide a referenceable platform for the delivery of other therapeutic agents with a narrow therapeutic window.

PMID 42929058
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-26

Phosphate-Engineered DNA Reporters Boost CRISPR-Cas12a Trans-Cleavage for Rapid and Sensitive Nucleic Acid Detection.

Yang Rui R, Guo Chong C, Pei Minjie M, Zhang Jiongyu J et al.

CRISPR-Cas12a molecular diagnostics rely on target-activated collateral cleavage of single-stranded DNA (ssDNA) reporters to generate fluorescence signals, yet the mechanisms governing reporter substrate processing remain poorly understood. Here we show that Cas12a trans-cleavage involves both endonucleolytic cleavage and exonucleolytic trimming. We further demonstrate that terminal phosphate modification of ssDNA substrates accelerates substrate cleavage activity and modulates trans-cleavage kinetics, thereby enhancing fluorescence output. Guided by this mechanistic insight, we engineered fluorophore-quencher ssDNA reporters bearing terminal phosphate modifications and identified a 3'-phosphate-engineered reporter that enables faster signal generation and higher fluorescence intensity. Incorporation of the engineered reporter into the CRISPR-Cas12a system enabled the development of Phos-CRISPR (Phosphate-engineered DNA reporters boost CRISPR), a rapid, sensitive, and specific nucleic acid detection platform that achieves results within 20 min, approximately threefold faster than conventional CRISPR assays. Applied to herpes simplex virus 1 detection, the Phos-CRISPR combined with recombinase polymerase amplification achieved a limit of detection of 20 aM and accurately identified clinical swab samples. These findings provide a general framework for understanding Cas12a trans-cleavage activity and establish a mechanistically informed strategy for enhancing next-generation CRISPR diagnostics.

PMID 42928415
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PubMedOrganic & biomolecular chemistry2026-10-26

Base-mediated tandem photochemical rearrangement/ring-opening approach to α-ketoamides from 2-arylallomaltols.

Milyutin Constantine V CV, Komogortsev Andrey N AN

A concise one-pot synthesis of aroyl-containing α-ketoamides from 2-aryl-substituted allomaltols has been established. The transformation proceeds through a visible light induced anionic photorearrangement to 3-hydroxypyran-2-one intermediates, which undergo in situ secondary amine-promoted ring opening. The employed secondary amines play a dual role, serving both as bases for the generation of photoactive anions and as nucleophiles for the subsequent ring-opening step. This newly developed tandem strategy enables efficient access to a series of α-ketoamides from readily available allomaltol derivatives in yields of up to 87%. Notably, irradiation of the same substrates in the absence of base follows an alternative ESIPT-induced pyranone ring contraction pathway, generating unstable α-hydroxy-1,2-diketones that were trapped in situ with o-phenylenediamine to afford quinoxaline derivatives.

PMID 42929786
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PubMedDyslexia (Chichester, England)2026-10-26

'I Am a Person Before My Label': Exploring People's Perceptions of Different Discourses Associated With Dyslexia.

Macdonald Stephen J SJ, Pearson Amy A, Botha Monique M, Leigh Jennifer J et al.

Language plays a central role in shaping how dyslexia is understood and negotiated across education, employment and everyday life. While debates have historically focused on diagnosis, less attention has been given to how adults who identify as dyslexic interpret and evaluate the labels applied to them. This article examines dyslexic adults' perceptions of dyslexia-related and neurodiversity movement terminology, drawing on a UK mixed-methods survey of 166 participants who identified as dyslexic, with or without co-occurring neurodivergences. Quantitative findings reveal a clear hierarchy of label preference. Participants strongly favoured dyslexia-specific, identity-based terms such as 'dyslexic', while rejecting broader, deficit-centred labels including 'learning difficulty', 'specific learning disability' and 'specific learning disorder'. Qualitative analysis shows these preferences are shaped by experiences of stigma and misrecognition. The findings show that adoption of a neurodivergent label varies depending on whether participants have single or multiple neurodivergent identities. Those with dyslexia alone expressed greater ambivalence towards the label of neurodiversity. In contrast, dyslexic participants alongside autism or ADHD were more likely to adopt the label. The study highlights the importance of listening to dyslexic voices in debates about terminology. It cautions against deficit-based and overly generalised language which risks reproducing stigma rather than challenging oppression.

PMID 42928419
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-26

Bioengineered Stroma-Camouflaged Nanovesicles Disrupt the IDO1/CD276 Immunosuppressive Circuit to Reinvigorate Antitumor Immunity.

Zhang Ziqi Z, Luo Jing J, Zhang Mengdi M, Zhuang Jingying J et al.

The cooperative upregulation of IDO1 and the immune checkpoint CD276 in solid tumors establishes a dual immunosuppressive circuit that depletes tryptophan, accumulates kynurenines, and silences T-cells. We engineered fibroblast-mimetic nanovesicles (AM@UIO-BMS/DOX) that uniquely integrate stromal-camouflaged tumor accumulation, CD276 checkpoint blockade, and co-delivery of doxorubicin with the clinical IDO1 inhibitor BMS-986205. The fibroblast-derived membrane coating promotes accumulation in fibroblast-rich tumor regions, while surface-anchored anti-CD276 scFv enables precision tumor specific targeting and concurrent checkpoint neutralization. Within the tumor microenvironment, doxorubicin elicits immunogenic cell death, and BMS-986205 metabolically recalibrates the tryptophan-kynurenine equilibrium, relieving the metabolic suppression that otherwise blunts T-cell priming. In syngeneic tumor models, this bioengineered platform profoundly remodeled the immune microenvironment, as evidenced by a tripartite shift: enhanced dendritic cell maturation and cross-presentation, expansion of Granzyme B+ cytotoxic CD8+ T lymphocytes, and selective depletion of CD25+FoxP3+ regulatory T cells. This concerted action effectively converted immunologically "cold" tumors into an inflamed phenotype, overcoming intrinsic chemoresistance and adaptive immune evasion. Collectively, our findings establish that bioengineered stroma-camouflaged nanovesicles disrupt the dual IDO1/CD276 immunosuppressive circuit, enhancing antitumor immunity and offering a promising strategy to surmount chemo-immunotherapy resistance in advanced solid tumors.

PMID 42928435
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