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spaglumic acid (Alerbak / Naabak / Naaxia)

✓ Approved

Thea · Small Molecule · Small Molecule

What is spaglumic acid?

spaglumic acid is a small molecule developed by Thea. It is approved for therapeutic indications via others or topical.

Drug Profile

Brand NamesAlerbak, Naabak, Naaxia
CompanyThea
Drug ClassSmall Molecule
RouteOthers, Topical
StatusApproved
Sources: ClinicalTrials.gov, Thea

Therapeutic Indications

spaglumic acid is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Eye disordersConjunctivitis allergic✓ Approved

Related Research Articles

PubMedPakistan journal of pharmaceutical sciences2026-06-09

Fumaric acid regulates morphine tolerance in bone cancer pain through spinal MrgC receptor modulation.

Liu Sijie S, Tang Minghao M, Zhao Jing J, Zhang Lulu L et al.

Bone cancer pain (BCP) represents a debilitating complication that profoundly impacts patient quality of life and predisposes to psychological comorbidities, including depression and anxiety. To investigate the effect of fumaric acid on morphine tolerance in BCP via spinal MrgC receptors. This study adopted an in-vivo animal experiment design. The BCP mouse model was established and divided into the Vehicle group, the fumaric acid monotherapy group with different doses, the fumaric acid + morphine combination group, the normal saline + morphine control group and the fumaric acid + normal saline control group. Intervention is carried out through intrathecal administration. Pain behavior tests such as the threshold for mechanical foot retraction, the number of spontaneous foot lifts, the duration of foot lift protection and the latency period of cold pain foot retraction were evaluated. The expression level of MrgC protein in spinal cord tissue was detected by Western blotting and immunohistochemistry. Fumaric acid dose-dependently attenuated BCP and delayed morphine tolerance, with EC50 values of 69.18 mg/kg (mechanical) and 99.78 mg/kg (cold). Its effects correlated with downregulation of spinal MrgC expression. Fumaric acid alleviates BCP and delays morphine tolerance by down-regulating the expression of spinal MrgC receptors. MrgC receptors are potential new therapeutic targets.

PMID 42262207
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PubMedScientific reports2026-06-09

Paper-based laser-written CoO-graphene biosensor for wireless sweat uric acid detection.

Ganesan Vinod K VK, Lee Soon Poh SP, Low Jen Hahn JH, Lim Eng Hock EH et al.

Uric acid is a critical metabolic biomarker for gout, kidney dysfunction, and cardiovascular disease. Persistent hyperuricemia promotes monosodium urate crystal deposition, triggering recurrent gout flares, chronic joint damage, and systemic inflammation, while early and continuous uric acid monitoring enables timely therapeutic intervention and improved disease outcomes. However, conventional blood tests and enzymatic sensors, although reliable, remain invasive, laboratory-bound, and unsuitable for continuous or point-of-care monitoring. Herein, we report a sustainable one-step strategy to fabricate a non-enzymatic uric acid sensor by direct laser writing on cobalt-treated paper with 455 nm irradiation, producing cobalt oxide-infused graphene. Unlike conventional metal-functionalized laser-induced graphene (LIG), which typically requires multi-step processing and non-biodegradable polymeric substrates, the present approach employs a biomass-derived paper substrate and simultaneously generates conductive graphene and redox-active cobalt oxide nanostructures in a single photothermal process. Furthermore, the incorporated multivalent Co2⁺/Co3⁺ redox couples act as biomimetic active sites for uric acid oxidation, enabling a flexible low-energy electron-hopping mechanism and enhanced interfacial charge transfer. The resulting porous hybrid electrode provides abundant electroactive sites for efficient sensing performance. Integrated into a flexible near-field communication (NFC) tag, the resulting platform enables wireless, battery-free uric acid monitoring in human sweat. The fabricated sensor achieved a sensitivity of 9.96 µA·μM-1 and a detection limit of 1.08 μM for uric acid sensing. The mechanical robustness is confirmed by minimal resonance frequency variation under bending, shifting only from 13.525 MHz at 0° to 13.575 MHz at 180° (~ 0.37% relative change). This work establishes a low-cost, scalable, and environmentally sustainable route toward metal oxide-carbon hybrid biosensors, offering a promising pathway for wearable uric acid monitoring and next-generation point-of-care diagnostics.

PMID 42260149
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-06-09

Bile acids in Alzheimer's disease: a double-edged sword in gut-liver-brain signaling and neurodegeneration.

Basri Rehana R, Al-Kuraishy Hayder M HM, Alruwaili Mubarak M, Al-Gareeb Ali I AI et al.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) deposition, tau pathology, synaptic dysfunction, neuroinflammation, and metabolic impairment. Increasing evidence suggests that bile acids, traditionally recognized for their roles in lipid digestion and hepatic metabolism, act as endocrine signaling molecules that influence central nervous system (CNS) homeostasis. Through enterohepatic circulation and microbiota-dependent biotransformation, bile acid composition is dynamically regulated and can modulate peripheral metabolic and immune pathways with downstream effects on the brain. Notably, bile acid signaling via key receptors such as the farnesoid X receptor (FXR) and the Takeda G protein-coupled receptor 5 and G-protein-coupled bile acid receptor 1 (TGR5/GPBAR1) has emerged as a mechanistic bridge linking liver-gut physiology to neuroinflammatory and neurodegenerative processes. Altered bile acid profiles have been reported in AD and mild cognitive impairment, with accumulating findings suggesting that hydrophobic secondary bile acids may contribute to blood-brain barrier (BBB) disruption and neurotoxicity. In contrast, hydrophilic bile acids may exert neuroprotective and anti-inflammatory effects. In addition, bile acids drive the release of gut hormones such as glucagon-like peptide 1 (GLP-1) and fibroblast growth factor 19 (FGF19), highlighting indirect neurometabolic pathways relevant to cognition and neurodegeneration. This narrative review synthesizes current biochemical, experimental, and clinical evidence supporting a role for bile acid signaling in AD pathogenesis and progression. We discuss receptor-mediated pathways, microbiota-bile acid interactions, neuroimmune modulation, and translational perspectives, proposing that bile acid-based biomarkers and therapeutic strategies targeting FXR/TGR5 signaling may represent promising avenues for future AD intervention.

PMID 42259980
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PubMedUlusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES2026-06-09

Role of maslinic acid in ischemia-reperfusion-induced testicular injury in rats.

Wei Si-Ming SM, Huang Yu-Min YM

The pathophysiology of testicular ischemia-reperfusion is characterized by a marked increase in reactive oxygen species. Oxidative damage caused by reactive oxygen species to cellular components, including DNA, proteins and lipids, leads to injury of spermatogenic cells. Maslinic acid, a bioactive compound found in Olea europaea, hawthorn, and other medicinal plants, exhibits antioxidant properties. This study aimed to determine whether maslinic acid protects testicular sperm production following ischemia-reperfusion injury in a rat model. Male rats were randomly assigned to three groups: a control group (Group 1), an ischemia-reperfusion group (Group 2), and an ischemia-reperfusion + maslinic acid group (Group 3). Ischemia was induced in the left testis by two-hour torsion, followed by reperfusion via surgical detorsion. The treatment group received intraperitoneal administration of maslinic acid at the onset of detorsion procedure. Following detorsion, left orchiectomy was performed at either four hours or three months. To comprehensively assess testicular oxidative stress and function, we measured key indicators: malondialdehyde concentration (reflecting reactive oxygen species levels); activities of superoxide dismutase and catalase, representing components of the cellular antioxidant system; and overall spermatogenic efficiency. These parameters were evaluated using biochemical assays and histological analysis with hematoxylin-eosin staining. Testicular ischemia-reperfusion significantly increased malondialdehyde levels while suppressing key antioxidant defenses (superoxide dismutase and catalase) and impairing spermatogenic function (p<0.001). Despite testicular damage induced by ischemia-reperfusion, maslinic acid treatment produced a partial restoration of these markers (p<0.01). In summary, maslinic acid mitigates ischemia-reperfusion-induced testicular injury by enhancing superoxide dis-mutase and catalase activities while reducing reactive oxygen species.

PMID 42261858
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PubMedAnnals of African medicine2026-06-09

Effect of Zoledronic Acid on Pain and Bone Mineral Density in Osteoporosis: A 2-year Longitudinal Study.

Kotian Prem P, Rajasekharan Pranav P, Gadwal Prafulla P, Agarwal Prananshu P et al.

Osteoporosis is a common metabolic bone disorder associated with reduced bone mineral density (BMD) and increased risk of fractures and chronic pain. Zoledronic acid (ZA), a bisphosphonate, is widely used in the management of osteoporosis because of its antiresorptive properties. To evaluate the effect of zoledronic acid on pain levels and bone mineral density in patients with osteoporosis over a 2-year follow-up period. A hospital-based observational pre-post study was conducted among 120 diagnosed osteoporosis patients. Each participant received a single dose of zoledronic acid and was followed for 2 years. Pain levels were assessed using the Visual Analog Scale (VAS), and BMD measurements were recorded at baseline and at structured 6-monthly intervals up to 2 years. Participants demonstrated higher pain scores at baseline, followed by a progressive decline at 6 months, 1 year, 1.5 years, and 2 years. This decreasing trend was statistically significant (P = 0.001). Similarly, BMD was lowest at baseline and showed a consistent increase across all follow-up intervals, with the upward trend also reaching statistical significance (P = 0.001). Zoledronic acid effectively reduces osteoporosis-related pain and significantly improves bone mineral density over time in patients with osteoporosis.

PMID 42260740
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PubMedUltrasonics sonochemistry2026-06-09

Mechanisms of ultrasonic enhanced co-leaching of U and REEs from low-grade uranium resources.

Zeng Jiahui J, Liu Chao C, Li Mu M, Ma Yuehui Y et al.

Uranium (U) and rare earth elements (REEs) are both strategic metallic elements. With the consumption of high-grade mineral resources, it is necessary to enhance the utilization of complex low-grade resources. This study proposes an ultrasonic-enhanced alkali pretreatment - acid leaching process for the recycling of uranium tailings associated with REEs. The ultrasonic-assisted alkaline pretreatment effectively disrupted the gangue structure by dissolving a portion of silicon (3.66%) and aluminum (5.59%). This enhanced the accessibility of metals encapsulated within the gangue minerals and altered the speciation of residual REEs, thereby facilitating the subsequent acid leaching of both U and REEs. The advantageous regions for acid leaching of U and REEs were identified through thermodynamic analysis. Effects of ultrasonic-assisted acid leaching conditions on the leaching efficiencies of U and REEs were investigated. The optimized acid leaching conditions are as follows: HCl concentration of 2.5 mol/L, leaching temperature of 70 °C, leaching time of 2 h, L/S ratio of 10:1, H2O2 addition of 5%, and ultrasonic power of 400 W with frequency of 40 kHz. The leaching efficiencies of U and REEs reached 90.43% and 72%, which increased by 17.09% and 12.33% respectively, compared to conventional leaching. The characteristics of the residue before and after ultrasonic leaching were compared to analyze the leaching mechanism. During acid leaching, the free radical capture experiment found that the ultrasonic effect promoted the decomposition of hydrogen peroxide to produce more free radicals, oxidizing insoluble U(IV) to dissolved U(VI). The ultrasonic effects strengthened the leaching kinetics for both U and REEs. The results provide an enhanced method for the efficient utilization of low-grade encapsulated mineral resources.

PMID 42259003
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