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HY

hyaluronic acid (BioHy / Euflexxa / BioLon)

✓ Approved

Johnson & Johnson Services, Inc. · therapeutic agent

What is hyaluronic acid?

hyaluronic acid is a therapeutic agent developed by Johnson & Johnson Services, Inc.. It is approved for therapeutic indications via injectable (others) or intraarticular injection.

Drug Profile

Brand NamesBioHy, Euflexxa, BioLon
CompanyJohnson & Johnson Services, Inc.
RouteInjectable (Others), Intraarticular Injection
StatusApproved
Sources: ClinicalTrials.gov, Johnson & Johnson Services, Inc.

Therapeutic Indications

hyaluronic acid is developed for 4 unique indications across 3 therapeutic areas.

Therapeutic AreaConditionPhase
Eye disordersGlaucoma✓ Approved
Musculoskeletal and connective tissue disordersOsteoarthritis✓ Approved
Surgical and medical proceduresAdjuvant therapy✓ Approved
Eye disordersDry eyePhase II

Related Research Articles

PubMedFrontiers in aging2026-10-15

Synovial fluid-derived extracellular vesicles modulate joint cell function in osteoarthritis.

Compañ Alvaro A, Carrabs Vittoria V, Ferrándiz María Luisa ML, Silvestre Antonio A et al.

Osteoarthritis (OA) is an age-related joint disease characterized by chronic inflammation and extracellular matrix degradation. Extracellular vesicles (EVs) in synovial fluid (SF) may modulate intercellular communication and influence disease progression. SF, cartilage, and synovial tissue were collected from knee OA patients (n = 68). SF-derived EVs (SF-EVs) were isolated by size exclusion chromatography and characterized by transmission electron microscopy (TEM), tunable resistive pulse sensing (qNano), and ELISA analysis of EV-associated markers (CD9, CD81, TSG101, and PDCD6IP) and the negative marker calnexin. In vitro experiments were performed using primary synoviocytes and chondrocytes stimulated with interleukin (IL)-1β in the presence or absence of SF-EVs. Inflammatory and catabolic markers were measured. SF-EVs (∼261 nm; ∼7 × 108 particles/mL) expressed canonical EV markers. In synoviocytes, SF-EVs reduced IL-1β-induced proliferation and decreased IL-6 and MMP-3 while increasing hyaluronic acid (HA). In chondrocytes, SF-EVs reduced IL-6 and MMP-13 and enhanced HA and IL-1Ra production, with sustained effects over time. These findings suggest that SF-EVs can modulate inflammatory and matrix-related responses in joint-resident cells under IL-1β-induced inflammatory conditions. Their distinct effects on synoviocytes and chondrocytes highlight the potential role of SF-EVs in regulating cell-specific responses within the osteoarthritic joint and warrant further investigation into their contribution to OA pathophysiology.

PMID 42876626
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PubMedJournal of materials chemistry. B2026-10-15

Mitochondria-targeted ROS-scavenging nanoreactor with dual-drug-loaded carbon dots for osteoarthritis therapy.

Li Weikun W, Luo Jinyuan J, Liang Shuiqi S, Zhong Qian Q et al.

Osteoarthritis (OA) pathology entails complex interactions among oxidative stress, chronic inflammation, cartilage degradation, and dysregulation of subchondral bone remodeling. Current therapeutic agents suffer from limited efficacy due to poor joint targeting and low bioavailability, highlighting the critical need for advanced drug delivery systems. In this study, a mitochondria-targeting reactive oxygen species (ROS)-scavenging nanoreactor (A@HP@SH/T) was developed for multi-mechanism OA repair. The nanoreactor is constructed using hollow mesoporous prussian blue (HMPB) as the carrier, loaded with carbon dots (AA CDs) co-assembled from astragaloside IV (AS-IV) and alendronate sodium (ALN), coated with diselenide-modified hyaluronic acid (Se-Se HA), and further conjugated with the mitochondrial-targeting ligand TPP. Through a temporal cascade of TPP-mediated mitochondrial anchoring, Se-Se HA ROS-responsive cleavage, and HMPB-mediated in situ protection and sustained release, AA CDs are precisely delivered to the lesion site, where they efficiently scavenge ROS and modulate mitochondrial homeostasis, thereby fundamentally breaking the vicious cycle of oxidative stress, chronic inflammation, and cartilage degradation within the joint. Additionally, the ALN component in AA CDs targets subchondral bone and modulates bone metabolism to reshape the local microstructure, offering both mechanical support and a beneficial nutritional microenvironment for cartilage regeneration. Both in vitro and in vivo studies confirmed that this system effectively restores mitochondrial homeostasis, alleviates inflammation, promotes cartilage differentiation, and regulates bone metabolism, thereby promoting OA repair. Collectively, this nanoreactor represents a highly promising strategy for the treatment of osteoarthritis.

PMID 42876417
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PubMedNatural product reports2026-10-15

γ-Amino acid-containing natural products of bacterial origin: structure, biosynthesis, and bioactivity.

Götze Sebastian S, Decker Tanya T, Balluff Sven S, Beemelmanns Christine C

Covering: 1966 to 2026γ-Amino acids are structurally diverse non-proteinogenic building blocks that endow bacterial natural products with unique conformational, physicochemical, and biological properties. Although individual γ-amino acid-containing metabolites have been extensively investigated, their structural diversity, biosynthetic origins, and functional significance have rarely been considered from a unified perspective. Here, we review nearly six decades of research on bacterial γ-amino acid-containing natural products, covering from 1966 and the discovery of bleomycin to genome-guided discoveries in 2026. We discuss the major structural classes of γ-amino acids, including GABA-derived, β-keto, statine-type, vinylogous, fully reduced, and masked amino acid-derived motifs, and highlight how these building blocks are generated through primary metabolism, hybrid NRPS-PKS assembly lines, and specialized tailoring reactions. Particular emphasis is placed on the relationships between γ-amino acid structure, biosynthetic logic, and biological function, including their roles in protease inhibition, covalent target engagement, metallophore activity, and microbial ecology. Finally, we discuss emerging opportunities for genome mining and biosynthetic engineering that are expected to accelerate the discovery and exploitation of γ-amino acid-containing natural products.

PMID 42876392
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PubMedAnimal bioscience2026-10-15

Nutritional and metabolic mechanisms linking low protein and low amino acid diets to fatty liver in laying hens.

Murai Atsushi A, Yamazaki Misae M, Furukawa Kyohei K

Fatty liver is a common metabolic disorder in laying hens and is strongly influenced by dietary protein and amino acid supply. Low protein or low amino acid diets disrupt the balance between nitrogen and energy intake, enhancing hepatic de novo lipogenesis. Severe dietary protein and amino acid deficiency also impairs hepatic apolipoprotein synthesis and secretion. These metabolic alterations promote hepatic triglyceride accumulation and increase susceptibility to fatty liver. Although nutrient-sensing mechanisms in birds remain incompletely defined, evidence from mammalian studies suggests that amino acid deficiency may activate GCN2-ATF4 signaling and modulate mTORC1 activity, contributing to lipogenic reprogramming. Importantly, protein dilution alone rarely induces severe steatosis; rather, the combination of low protein and excessive dietary energy (HELP diet feeding) markedly amplifies lipogenesis, oxidative stress, inflammation, and hepatic injury, accelerating progression toward fatty liver hemorrhagic syndrome (FLHS). This review summarizes current knowledge on the physiological and molecular mechanisms linking low protein and low amino acid diets to fatty liver in laying hens, evaluates the HELP model as an experimental framework for FLHS, and outlines nutritional and functional additives shown to mitigate HELP-induced hepatic pathology. Together, these insights provide a mechanistic basis for developing safer low protein feeding strategies in modern layer production.

PMID 42875912
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PubMedFrontiers in physiology2026-10-15

Ceramidase is involved in metabolic reprogramming of fibroblasts under hypoxia conditions.

Terlizzi Michela M, D'Andria Emmanuel E, Colarusso Chiara C, Di Caprio Simone S et al.

Physiological metabolic reprogramming is a cells strategy to resist/counteract stress to preserve homeostasis. Hypoxia is an important stress stimulus that can promote tissue remodeling and fibrosis, in which alterations in sphingolipid metabolism may contribute to fibroblast responses. Here, we investigated the potential role of acid ceramidase (ASAH1), a key enzyme of the sphingolipid salvage pathway, in fibroblast adaptation to hypoxic stress. Human fibroblasts were exposed to hypoxia for 24, 48, and 72 hours, and metabolic and redox changes were investigated following pharmacological inhibition of acid ceramidase with D-Nmappd. These findings were complemented by analyses of publicly available bulk and single-cell RNA sequencing datasets from idiopathic pulmonary fibrosis (IPF) lungs. Hypoxic fibroblasts showed metabolic remodeling involving glucose-, amino acid-, and redox-associated pathways, together with changes consistent with an adaptive antioxidant response, including alterations in the GSH/GSSG balance. Pharmacological inhibition of acid ceramidase under hypoxia was associated with changes in carnitine metabolism and long-chain fatty acid β-oxidation, reduced GSH and GSSG levels, and decreased expression of Nuclear Factor Erythroid 2-Related Factor 2 (NRF2), Superoxide dismutase 2 (SOD2), and 8-Oxoguanine DNA Glycosylase 1 (OGG1). In IPF lung tissue, ASAH1 expression was associated with glycolytic and redox-related genes. Single-cell analysis showed that ASAH1-expressing IPF fibroblasts were enriched in transcriptional programs related to hypoxic responses and oxidative stress regulation and displayed features associated with a less activated phenotype. Overall, these findings suggest that acid ceramidase/ASAH1 is associated with fibroblast metabolic and redox adaptation to hypoxic stress and may influence fibroblast activation in IPF.

PMID 42876482
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PubMedNature communications2026-10-15

Early coconut oil exposure suppresses chronic experimental Crohn's disease via myristic acid and enhanced regulatory T cells.

Rodriguez-Palacios Alex A, Raffner Basson Abigail A, Menghini Paola P, Ezeji Jessica J et al.

Public health advisory guidelines caution against the consumption of saturated fats, especially coconut oil (CO), yet CO is widely consumed in regions with low inflammatory bowel disease prevalence (IBD) and is often perceived as beneficial by IBD patients. CO is rich in medium-chain saturated fatty acids, notably lauric acid (C12:0) and myristic acid (C14:0) which are negligible in mammalian tissues without dietary intake. Because IBD is linked to saturated fats consumption, here we tested and unexpectedly found that CO and its saturated fatty acids are beneficial suppressing intestinal inflammation in SAMP1/YitFc mice, a chronic IBD model of Crohn's disease-like ileitis. In young mice, the early exposure to a high-dose CO-based diet prevented ileitis in 63.64% of animals (95%CI = 30.79-to-89.07%). Importantly, comparable protection was observed at lower doses amenable for human translation. Although CO did not reverse established disease in adult mice, when combined with steroids, it prolonged the period of steroid-induced remission illustrating its therapeutic benefits in IBD. Disease prevention was associated with myristic acid and correlated with anti-inflammatory microbiota shifts and enhanced regulatory T-cell responses, without adverse effects. Findings challenge current dietary advisories against CO and support reevaluation of CO and myristic acid as anti-inflammatory dietary adjuvants for the prevention and management of established IBD.

PMID 42875437
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