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ibuprofen + arginine (Spedifen / Zafen / Espedifen)

✓ Approved

Zambon · PTGS1 · 小分子

什么是 ibuprofen + arginine?

ibuprofen + arginine 是一种小分子,由Zambon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Spedifen, Zafen, Espedifen
公司Zambon
药物类别小分子
分子靶点PTGS1, PTGS2
给药途径Oral (PO)
状态Approved

作用机制

分子靶点

ibuprofen + arginine 作用于 2 个分子靶点:

PTGS1prostaglandin-endoperoxide synthase 1 (COX3, PCOX1)
PTGS2prostaglandin-endoperoxide synthase 2 (GRIPGHS, hCox-2)
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

ibuprofen + arginine 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
Gastrointestinal disordersAbdominal pain✓ Approved
Hepatobiliary disordersHepatitis✓ Approved

相关研究文献

PubMedCardiology in the young2026-08-05

Minimising an outpatient medication regimen after paediatric cardiac surgery.

Penk Jamie Smith JS, Jackson Lindsay L, Baptista de Faria Guilherme G, Doyle Laura L et al.

We implemented a quality improvement initiative to optimise the outpatient medication regimen after paediatric cardiac surgery. A previous trial that limited furosemide found no readmissions for pleural effusion but an increase in pericardial effusions. A similar quality improvement project had implemented prophylactic non-steroidal anti-inflammatory drugs and found a decrease in readmissions for pericardial effusion. We used these results to design an outpatient medication regimen that minimises furosemide and uses only targeted ibuprofen and report readmission rates from this project. Single-centre analysis of outcomes since the adoption of a quality improvement initiative aiming to limit outpatient diuretics (≤5 days) while using targeted ibuprofen to prevent pericardial effusion readmissions. Two hundred and one patients were eligible for analysis. Forty-one patients (20.4%) were prescribed >20 days of diuretics due to compliance failure and were not considered to have received a limited diuretic regimen, leaving 160 patients. Of those, 53 (33.1%) were correctly prescribed targeted ibuprofen based on meeting "high-risk" criteria. There was one readmission for pleural effusion and 2/160 (1.3%) readmissions for pericardial effusion. The previous prospective study of limited furosemide without ibuprofen had a pericardial effusion readmission rate of 4/61 (6.6%) versus the 2/160 (1.3%) after implementing the regimen described in this report (p = 0.04). We describe a medication regimen using limited outpatient furosemide without increased readmissions for pleural effusions. Targeted ibuprofen was used for high-risk patients only, and there were fewer readmissions for pericardial effusions than in a previous trial that used furosemide alone.

PMID 42553008
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PubMedAdvanced materials (Deerfield Beach, Fla.)2026-08-05

A Metabo-Reprogramming Niche Remodeling System Halts Osteoarthritis by Restoring the FGF21-Arginine Axis.

Pan Hao H, Zhu Haoze H, Huang Siman S, Chen Likai L et al.

Osteoarthritis (OA), a global leading cause of chronic pain and disability, lacks disease-modifying osteoarthritis drugs (DMOADs) targeting its core pathogenesis. scRNA-seq of human OA cartilage showed marked depletion of a high-arginine-metabolism chondrocyte subpopulation driving cartilage degeneration, with its key upstream regulator FGF21, significantly downregulated in OA cartilage. Mechanistically, FGF21 rescues IL-1β-induced chondrocyte dysfunction via ASS1/ASL -mediated arginine biosynthesis, an effect abrogated by ASS1 knockdown, confirming the FGF21-arginine pathway's role and FGF21 as a therapeutic target. Guided by this mechanism, we engineered a hydrogel-based bioinspired metabo-reprogramming niche remodeling system (MetaRemod) to achieve precise and efficient delivery of FGF21 to OA chondrocytes. In a mouse OA model, MetaRemod effectively halted OA progression by sustaining targeted delivery of bioactive FGF21, restoring chondrocyte arginine metabolism, preserving cartilage structure and joint space, restoring subchondral bone integrity, and mitigating synovitis. Critically, scRNA-seq of treated cartilage confirmed the restoration of the depleted "high-arginine-metabolism" chondrocyte subpopulation, directly validating that MetaRemod reverses OA's core metabolic defect. This study establishes the FGF21-arginine metabolic axis as a key therapeutic target for OA and validates MetaRemod as a promising strategy that synergizes targeted FGF21 delivery and metabolic reprogramming, laying a solid foundation for the clinical translation of metabolic reprogramming-based DMOADs.

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PubMedAdvanced healthcare materials2026-08-05

Engineering Concentration-Dependent Intravitreal Mobility via Cyclic Arginine-Enriched Nanocarrier Surface Modification: In Vivo Proof-of-Concept in a Porcine Large Animal Model.

Hammer Maximilian M, Ackermann Bryan Calder BC, Stoß Anna A, Junker Niklas N et al.

Nanoparticulate drug delivery systems represent a promising platform for sustained intraocular drug release following intravitreal administration, leveraging low metabolic turnover of the vitreous to maintain therapeutic drug levels over extended periods. Despite this potential, nanoparticle diffusion toward the visual axis can induce light scattering and visual disturbance. Given the negative charge of the vitreous, surface-engineered nanoparticles provide a strategy to modulate particle mobility and restrict off-target migration. Here, we performed a 6-week in vivo evaluation in pigs of an intravitreally applied, positively charged, cyclic-arginine surface-functionalized liposomal nanocarrier designed to reduce intravitreal mobility. Three formulations containing 0.1%, 0.5%, or 1% cyclic-arginine-modified phospholipid were compared with unmodified control liposomes in a large animal pig model. A multimodal biocompatibility and performance assessment was conducted, including intraocular pressure monitoring, fundus imaging, structural and angiographic OCT, dye-based angiography, and post-mortem retinal immunostainings. Cyclic-arginine surface functionalization of the liposomes resulted in a concentration-dependent reduction in intravitreal mobility, quantified by vitreous haze and fundus-based distribution analyses. All surface-engineered nanoparticles demonstrated excellent ocular biocompatibility without structural or vascular adverse effects. These data establish cyclic-arginine surface modification as a robust design principle to modulate intravitreal mobility and support the development of next-generation nanoparticle biomaterials for long-acting ophthalmic drug delivery.

PMID 42554203
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PubMedeLife2026-08-05

Microenvironmental arginine restriction sensitizes pancreatic cancers to polyunsaturated fatty acids by suppression of lipid synthesis.

Jonker Patrick B PB, Sadullozoda Mumina M, Cognet Guillaume G, Apiz Saab Juan J JJ et al.

Nutrient limitation is a characteristic feature of poorly perfused tumors. In contrast to well-perfused tissues, nutrient deficits in tumors impose metabolic constraints on cancer cells. The metabolic constraints created by the tumor microenvironment can lead to vulnerabilities in cancers. Identifying the metabolic constraints of the tumor microenvironment and the vulnerabilities that arise in cancers can provide new insight into tumor biology and identify promising anti-neoplastic targets. To identify how the microenvironment constrains the metabolism of pancreatic tumors, we challenged pancreatic cancer cells with microenvironmental nutrient levels and analyzed changes in cellular metabolism. We found that arginine limitation in pancreatic tumors perturbs saturated and monounsaturated fatty acid synthesis by suppressing the lipogenic transcription factor SREBP1, in part via activation of the amino acid sensor GCN2. Synthesis of these fatty acids is critical for maintaining a balance of saturated, monounsaturated, and polyunsaturated fatty acids (PUFAs) in cellular membranes. Because of microenvironmental constraints on fatty acid synthesis, pancreatic cancer cells and tumors are unable to maintain lipid homeostasis when exposed to PUFAs, leading to cell death by ferroptosis. In sum, arginine restriction in the tumor microenvironment constrains lipid metabolism in pancreatic cancers, which renders these tumors vulnerable to polyunsaturated-enriched fats.

PMID 42554218
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PubMedHIV/AIDS (Auckland, N.Z.)2026-08-05

From Denial to Near Blindness: Overcoming Herpes Zoster Ophthalmicus in a Rural Ugandan Man with HIV and Alcoholism.

Okongo Benson B, Amuge Gladys G, Adong Ruth Lucy RL, Okengo Anthony O AO et al.

In remote Ugandan settings, HIV care retention remains poor among men and pastoralists. Despite progress toward UNAIDS 95-95-95 targets, structural barriers, geographic isolation and stigma continue to undermine long-term retention. In 2022, a male pastoralist in his early forties with heavy alcohol use presented to a rural health center in Karamoja with fever and weight loss, and was diagnosed with HIV. He declined antiretroviral therapy (ART) believing the drugs were "poisonous" and was lost to follow-up for 48 months. He re-presented in March 2026 with a one-year history of a scaly, pruritic lesion on his right hand extending to the face and neck, unresponsive to antifungal creams. Two days prior, he developed an acutely painful vesicular eruption in the right V1 trigeminal distribution, along with oropharyngeal candidiasis. CD4 count was 120 cells/μL and urine TB LAM was positive, indicating disseminated tuberculosis. While LAM is highly suggestive and warrants immediate empirical treatment, definitive diagnosis of dissemination ideally requires clinical and radiological correlation. He was treated with oral acyclovir (800 mg five times daily for 10 days), topical acyclovir, ibuprofen, intensive-phase anti-TB therapy, and fluconazole (200 mg daily for 14 days). ART was deferred for two weeks to manage acute opportunistic infections and monitor for IRIS. At two weeks, the zoster lesions had crusted, oral candidiasis cleared, and pain reduced to 2/10. ART was initiated on day 14 with village health team support. At three months, he remained adherent with no new opportunistic infections. Delayed ART initiation caused years of preventable suffering. This case highlights the urgent need in low-income settings for community re-engagement strategies, integrated HIV/co-infection screening, point-of-care diagnostics, and culturally tailored care. As the patient stated: "I was sick, and now I am well. The science of HIV treatment is a miracle, and I am living proof.".

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PubMedJournal of the science of food and agriculture2026-08-05

Pasteurized Akkermansia muciniphila AKK PROBIO ameliorates inflammation and metabolic disorder in db/db mice with alterations in gut microbiota and hepatic TLR4/NF-κB and SREBP2/HMGCR signaling.

Chen Mengling M, Li Rao R, Xiang Yangling Y, Ma Xin X et al.

Diabetes mellitus, especially type 2 diabetes mellitus (T2DM), represents a significant global health challenge. Growing evidence indicates that Akkermansia muciniphila, a promising next-generation beneficial microorganism, could help alleviate metabolic disorders. Nevertheless, its strain-specific effects and associated mechanisms require further investigation. Here, we investigated the potential effects of pasteurized A. muciniphila AKK PROBIO in T2DM using db/db mice. Our findings show that pasteurized AKK PROBIO supplementation was associated with lower fasting glucose levels, reduced inflammatory markers, and improved cholesterol balance in db/db mice. Pasteurized AKK PROBIO administration was accompanied by changes in gut microbiota composition, including enrichment of bacterial taxa linked to short-chain fatty acid (SCFA) production, and by increased GLP-1 levels and altered serum metabolites, including 9,9'-di-cis-ζ-carotene and l-arginine. These changes were paralleled by reduced hepatic expression of proteins related to the TLR4/MyD88/IKKα/NF-κB and SREBP2/HMGCR signaling pathways. Taken together, our findings indicate that pasteurized AKK PROBIO ameliorates metabolic disorder and inflammation in db/db mice, accompanied by changes in gut microbial ecology, serum metabolites, and hepatic inflammatory/lipid metabolic signaling. This study supports pasteurized A. muciniphila AKK PROBIO as a postbiotic for further investigation in metabolic disorders. © 2026 Society of Chemical Industry.

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