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hyaluronic acid (Provisc)

✓ Approved

Novartis AG · therapeutic agent

What is hyaluronic acid?

hyaluronic acid is a therapeutic agent developed by Novartis AG. It is approved for therapeutic indications.

Drug Profile

Brand NamesProvisc
CompanyNovartis AG
StatusApproved
Sources: ClinicalTrials.gov, Novartis AG

Therapeutic Indications

hyaluronic acid is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Surgical and medical proceduresAdjuvant therapy✓ Approved
Eye disordersDry eyePreclinical

Related Research Articles

PubMedClinical oral implants research2026-07-17

Effect of Hyaluronic Acid on Palatal Wound Healing-A Randomized Crossover Clinical Trial.

Dahi Madeleine M, Amash Sara S, Bertl Kristina K, Beck Florian F et al.

To assess the effect of a hyaluronic acid (HyA) containing gel on patient-related outcomes (PRO) and wound healing after palatal punch-biopsy representing a free gingival graft. A punch-biopsy (6 mm diameter, 2 mm thickness) was harvested from one side of the palate at Day 0 and from the contralateral side at Day 21. Sites were randomly allocated to either 0.3% HyA containing gel (test) or sterile saline solution (control), professionally applied after harvesting and then self-applied three times/day for 7 days. Up to 21 days PRO-related questionnaires were answered and intraoral scans and photographs recorded to assess wound re-epithelialization, tissue refill, and color match. Eighteen of 25 recruited participants were analyzed. Pain perception, difficulties with eating/drinking, and taste alterations significantly decreased over time and were hardly experienced after Day 7 in both groups (p > 0.05). Participants reported significantly more often a positive experience after applying HyA compared to placebo, that is, in 8 versus 1 out of 18 cases. The residual wound area was significantly smaller in the test compared to control group at Day 7, and cases with a thicker palatal tissue showed tendency for faster re-epithelialization. Despite the potential limitations of the present study (i.e., possibility of a carryover effect, questionable blinding of the participants), repeated local application of a 0.3% HyA containing gel appears to only accelerate re-epithelialization in an open palatal wound and provide a positive experience after application, but it did not improve any PRO in such small-sized wounds compared to sterile saline application. ClinicalTrials.gov identifier: NCT05099718.

PMID 42464383
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PubMedAdvanced materials (Deerfield Beach, Fla.)2026-07-17

Chessboard Microneedle Array for Inflammation Regulation via Spatiotemporally Controlled Drug Delivery.

Jiang Yechun Y, Gou Yongqi Y, Shen Hui H, Wang Yidie Y et al.

Excessive production of reactive oxygen species during photodynamic therapy (PDT) can exacerbate inflammation at the infection site and increase the risk of tumor metastasis, thereby posing significant challenges to treatment efficacy. In this study, a chessboard-structured microneedle patch (HPC@PCN CMN) was designed using a micromolding technique. This design spatially separates and encapsulates photosensitizers and antioxidants within distinct fast- and sustained-release microneedle systems, respectively, thereby achieving spatiotemporally ordered control of PDT and anti-inflammatory treatment. Additionally, by adjusting the crosslinking degree of hyaluronic acid, the release rate of antioxidant drugs can be regulated, which facilitates a prolonged anti-inflammatory effect. The results indicate that the anti-inflammatory process of HPC@PCN CMN can alleviate inflammation by inhibiting the ATP-P2RX4 pathway, demonstrating promising efficacy in the treatment of acne and melanoma. Overall, the developed chessboard microneedle platform is programmable, enabling not only the sequential regulation of oxidation-antioxidation but also the potential for broader applications in drug-delivery scenarios.

PMID 42466552
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PubMedDiscover nano2026-07-17

Green synthesized cobalt doped graphene quantum dots derived from Boswellia serrata for dual ligand targeted bioimaging and delivery of exemestane.

Harde Minal T MT, Ingle Rahul R, Dhamal Sakshi S, Deshmukh Prashant P et al.

Major objective of hydrothermal method is to achieve the synthesis of Cobalt doped Graphene quantum dots (Co-GQDs) using natural precursor (Boswellia serrata gum resin). The Co-GQDs were surface engineered with folic acid (FA) and hyaluronic acid (HA) to enable dual targeting module (Co-GQDFH), followed by loading of the anticancer drug Exemestane (EXE@Co-GQDs). The nanosized, crystallite structure with high luminescence intensity was maintained after functionalization and drug loading process was assessed from preliminary physicochemical analysis. The EXE@Co-GQDFH forms complex via passive loading approach and achieves and entrapment efficiency of 68.58%. The in-vitro drug release study shows extended release of EXE from the surface functionalized Co-GQDFH for 24 h and releases (~ 88%) maximum encapsulated drug. The dose dependent toxicity was observed for EXE@Co-GQDFH (49.5 µg/ml) on MCF-7 cell breast cancer cell types while IC50 value was comparable to 5-Fluorouracil. The fluorescent Co-GQD shows high bioimaging and cellular uptake efficiency in MCF-7 cells. The surface conjugation with FA and HA on Co-GQDs shows enhanced activity with zone of inhibition was found to be 25 mm while the Co-GQD shows 20 mm suggest conjugation improved the antimicrobial effect. Radical scavenging activity was also demonstrated, with Co-GQDs showing 77.92% and EXE@Co-GQDs was 59.02% DPPH inhibition. These results suggest that surface-engineered Co-GQDs offer a multidentate nanoplatform for targeted delivery, imaging, and therapy in breast cancer applications.

PMID 42467326
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PubMedJournal of dental research2026-07-17

DAPK1 Ablation Promotes Wound Healing by Keratinocyte Modulation.

Li Y Y, Hu M M, Yin H H, Cao Y Y et al.

Death-associated protein kinase 1 (DAPK1), a Ca²+/calmodulin-regulated serine/threonine kinase, plays a pivotal role in epidermal homeostasis, tissue repair, and cutaneous wound healing. However, its role in oral mucosal repair remains unclear. In this study, we established a global Dapk1 knockout mouse model to create 1.5-mm circular palatal wounds in mice aged 8 to 12 wk. Our results demonstrated that DAPK1 deficiency significantly accelerated oral wound closure. In vitro experiments further confirmed that DAPK1 modulates the proliferation and migration of human oral keratinocytes. Mechanistic investigations through transcriptome sequencing revealed activation of the Wnt signaling pathway in Dapk1 knockout mice following injury, characterized by pronounced upregulation of Wnt3, Fosl1, and Ctnnd2, alongside downregulation of innate immune mediators, including Il7, Ccl28, Ccr2, Ccl5, and Cxcr4. These findings suggest that loss of DAPK1 enhances epithelial proliferation and migration while attenuating local inflammation. Furthermore, we developed a novel microneedle patch for drug delivery, consisting of GelMA tips encapsulating the DAPK1 inhibitor (HS-38) and a hyaluronic acid substrate. This system facilitated efficient mucosal penetration and localized delivery. Application of the microneedle patch significantly improved wound healing in both normal and diabetic mouse models. Collectively, these findings uncover a previously unrecognized role of DAPK1 in oral mucosal repair and highlight its potential as a molecular target to accelerate wound healing.

PMID 42466657
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PubMedbioRxiv : the preprint server for biology2026-07-17

Expanding Microgel Parameters to Model the Tumor Microenvironment and Examine Temozolomide Resistance in Glioblastoma.

Payan Brittany A BA, Kattoor Joel J, Carrillo Diaz de Leon Annika A, Thompson Gunnar B GB et al.

Glioblastoma (GBM) is a highly aggressive brain tumor with a five-year survival rate of less than 5%. The current standard of care established 20 years ago includes maximal surgical resection and administration of alkylating agent temozolomide (TMZ). GBM is highly invasive, and GBM cells that evade surgical resection can become resistant to TMZ and develop new aggressive secondary tumors. Post-relapse there are few treatment options available to patients. Tissue engineering approaches suggest the opportunity to develop in vitro models of the GBM tumor microenvironment that may accelerate the discovery of novel therapies for GBM. Here, we report the adaptation of hydrogel microdroplets (microgels) to encapsulate GBM cells in a tailorable 3D matrix to assess patters of growth and to screen TMZ drug response using patient-derived xenograft (PDX) specimens. We exploit a unique aspect of the microgel system to account for the cellular heterogeneity within the tumor microenvironment (TME). We combine cell-laden microgels generated from TMZ-resistant and TMZ responsive variants of the same PDX specimens to create heterogeneous populations with varying levels of drug sensitivity. We demonstrate a range of drug resistance phenotypes as a function of the ratio of TMZ-responsive to resistance cells and identify the population required for TMZ-resistance to overtake take the response. We then investigate the influence of tumor mimetic shifts in hyaluronic acid bioavailability and hypoxia on patterns of TMZ resistance. We show exposure to matrix-bound hyaluronan increases TMZ resistance and the glioma stem cell population in both cell variants. Lastly, we report an increase in TMZ sensitivity but divergent changes in the GSC subfraction for TMZ resistant vs responsive GBM in the presence of hypoxia. Together, we demonstrate the versatility of cell-laden microgel approach to replicate heterogenous tumor populations, model shifts in the tumor microenvironment, and rapidly screen therapeutic response.

PMID 42465419
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PubMedColloids and surfaces. B, Biointerfaces2026-07-17

Dual-targeted pH-responsive nanoliposome (M5/NMN/DEAP/iRGD-Lip): Immunostimulatory-photodynamic synergy for breast cancer therapy.

Zhuang Junwei J, Guo Chen C, Ye Xingming X, Zhang Jingyuan J et al.

Photodynamic therapy (PDT) holds promise for combination antitumor therapies by triggering immunogenic cell death (ICD). ICD is defined as the process by which tumor cells, upon death induced by external stimuli, convert from a non‑immunogenic to an immunogenic state, thereby mediating an anti‑tumor immune response in the host. But the poor aqueous solubility and inadequate tumor targeting of photosensitizers hinder their clinical translation. This study focuses on a novel BODIPY photosensitizer (M5) and aims to improve its antitumor efficacy via efficient tumor-targeted delivery and controllable release. Herein, we successfully synthesized iRGD-functionalized DSPE-PEG2000-iRGD and pH-sensitive HA-g-DEAP polymers, and further fabricated multifunctional M5/NMN/DEAP/iRGD-Lip liposomes via the thin-film dispersion method, which possess pH responsiveness and enhanced tumor-targeting ability. β-Nicotinamide Mononucleotide (NMN), a NAD + precursor, exerts a potent stimulatory effect on T-cell activation; 3-(Diethylamino)propylamine (DEAP) and hyaluronic acid (HA) can form pH-responsive HA-g-DEAP; the iRGD peptide (CRGDK/RGPDC), upon hydrolysis at its C‑terminus, exposes a motif that binds to neuropilin‑1 (NRP1), thereby conferring tumor‑targeting and tissue‑penetrating properties, endowing the liposomes with tumor-targeting and tissue-penetrating capabilities. M5 exhibits a high molar absorption coefficient of 5.33 × 104 M⁻¹ cm⁻¹ and a singlet oxygen quantum yield of 0.3854. In vitro cellular assays showed IC50 values of 104.1 nM and 72.68 nM in breast cancer MDA-MB-231 and 4T1 cells, respectively. Treatment with M5/NMN/DEAP/iRGD-Lip induced apoptosis rates of 56.84% and 55.6% in MDA-MB-231 and 4T1 cells, respectively. T-cell co-culture assays showed that M5/NMN/DEAP/iRGD-Lip increased the proportions of CD4+ and CD8+ T cells while reducing the proportion of regulatory T cells (Tregs) among CD4+ T cells. Collectively, the multifunctional M5/NMN/DEAP/iRGD-Lip liposomes integrate targeted delivery, pH-controlled release, and synergistic PDT-immunotherapy, effectively addressing key limitations of conventional photosensitizers. This work provides a promising nanoplatform for the development of novel combination therapies against breast cancer, laying a foundation for future preclinical and clinical translations.

PMID 42462379
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