Drug Database
DE

desonide (Desonate / desonide Hydrogel / Desowen)

✓ Approved

SkinMedica, Inc. · NR3C1 · Small Molecule

What is desonide?

desonide is a small molecule developed by SkinMedica, Inc.. It is approved for therapeutic indications via topical.

Drug Profile

Brand NamesDesonate, desonide Hydrogel, Desowen
CompanySkinMedica, Inc.
Drug ClassSmall Molecule
Molecular TargetNR3C1
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, SkinMedica, Inc.

Mechanism of Action

Molecular Targets

desonide acts on 1 molecular target:

NR3C1nuclear receptor subfamily 3 group C member 1 (GR, GCCR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

desonide is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersDermatitis allergic✓ Approved
Skin and subcutaneous tissue disordersDermatitis atopic✓ Approved

Related Research Articles

PubMedFrontiers in medicine2026-06-08

Efficacy and safety of MuShengshu in the treatment of mild-to-moderate atopic dermatitis: protocol for a randomized, double-blind, placebo-controlled trial.

Gao Xiangjin X, Cai Ruiqi R, Lu Jinrong J, Duan Zhen Z et al.

Atopic dermatitis (AD) is a prevalent chronic and recurrent inflammatory skin disease. Guidelines for the treatment and care of AD suggest that appropriate bathing can facilitate the repair of skin lesions. MuShengshu is a weakly acidic bath solution that contains traditional Chinese medicine ingredients. Previous studies indicate its potential to alleviate pruritus and promote the healing of skin lesions in patients with dermatosis. However, high-quality evidence is still limited. This randomized, double-blind, placebo-controlled clinical trial aims to assess the efficacy and safety of MuShengshu (MSS) combined with foundational therapies in patients with mild-to-moderate AD. A total of 66 patients with mild-to-moderate AD will be enrolled at the Shanghai Skin Disease Hospital from August 2025 to June 2026. Patients will be randomly assigned in a 2:1 ratio to either the treatment group (MSS combined with foundational therapies, n = 44) or the control group (MSS placebo combined with foundational therapies, n = 22). Patients will receive MSS or MSS placebo once daily, for 4 months. Meanwhile, the foundational therapies include desonide cream for mild AD and triamcinolone acetonide cream for moderate AD, both of which will be applied twice daily for 2 weeks. Additionally, all patients will receive urea ointment twice daily for 4 weeks. The primary outcome indicator is EASI50, defined as the proportion of patients achieving ≥50% improvement in the Eczema Area and Severity Index (EASI) score at week 4 from baseline. The secondary outcome indicators include the EASI, Visual Analogue Scale (VAS), Investigator's Global Assessment (IGA), and Dermatology Life Quality Index (DLQI), which will be assessed at baseline (week 0), weeks 1, 2, 4, and 16. In this study, statistical analyses will be conducted using SAS 9.4 software, with statistical significance being defined as a two-tailed α level of 0.05. In this study, ethical approval was granted in March 2025, with registration completed in the International Traditional Medicine Clinical Trial Registry in June 2025. Recruitment of participants began in August 2025 and is anticipated to completed by June 2026. Data analysis is set to start in August 2026, with preliminary trial results expected to be submitted for peer-reviewed publication by December 2026. Findings in this study are expected to provide evidence for the incorporation of traditional Chinese herbal bath solutions into the comprehensive management of AD. https://www.chictr.org.cn/, Identifier ITMCTR2025001206.

PMID 42254381
Read full article →
PubMedInternational immunopharmacology2026-04-04

Rutin targets PD-L1 for the treatment of atopic dermatitis: network pharmacological analysis and experimental evidence.

Wang Mingxia M, Cheng Guangyuan G, Ma Xiaoxuan X, Xu Haotian H et al.

Atopic dermatitis (AD) is a chronic inflammatory skin disease with high prevalence, recalcitrant nature, and significant socio-economic burden. Rutin, a bioactive flavonoid abundant in traditional medicinal plants, has documented ethnomedical uses in inflammatory conditions and exhibits antioxidant, cytoprotective, and anti-inflammatory properties. Evidence suggests that topical application of rutin can ameliorate the symptoms of atopic dermatitis. However, its underlying therapeutic mechanism remains elucidated, necessitating further in-depth investigation. To explore the potential mechanisms of rutin on AD through network pharmacology and experiments. Potential targets and signaling pathways of rutin in AD treatment were identified via network pharmacology. In vitro, cell viability of rutin was evaluated using the CCK8 assay (Cell Counting Kit-8), and the expression of inflammatory factors was detected by RT-qPCR. In vivo, the therapeutic efficacy of rutin was assessed in calcipotriol (MC903)-induced AD-like mouse models. Immunofluorescence was performed to confirm PD-L1 as the core target. The binding interaction between rutin and PD-L1 was verified by Cellular Thermal Shift Assay (CETSA) and Surface Plasmon Resonance (SPR). Finally, shPD-L1 lentiviral infection of Normal Human Epidermal Keratinocytes (NHEK) was conducted to validate that rutin exerts anti-inflammatory effects through PD-L1. Network pharmacology identified PD-L1 signaling pathway as rutin's core pathway in AD treatment. In vitro, CCK-8 assay revealed that the IC₅₀ of rutin in NHEKs was 17.51 μM, 10 μM rutin significantly downregulated TSLP/CCL17 mRNA in TII-stimulated NHEKs. In vivo, 1.5% rutin cream best ameliorated MC903-induced AD-like lesions in mice, reducing EASI scores, scratching bouts, and epidermal thickness, comparable to desonide; IHC showed upregulated epidermal PD-L1. Target validation: immunofluorescence confirmed PD-L1 co-localization with cytokeratin 14 (CK14), CETSA enhanced PD-L1 stability, SPR verified specific binding (KD = 2.53 × 10-6 M). shPD-L1 lentiviral infection of NHEKs confirmed rutin's anti-inflammatory effect is PD-L1-dependent. In summary, this study elucidates a novel mechanism by which rutin ameliorates AD-like inflammation through direct binding and upregulation of PD-L1, leading to enhanced epidermal expression and subsequent immunomodulation. Moreover, compared to conventional medications, rutin effectively reduces TEWL and strengthens the skin barrier. These findings not only advance our understanding of rutin's pharmacological activity but also support the continued investigation of natural compounds as targeted therapeutic agents for inflammatory skin diseases. The convergence of traditional knowledge and modern mechanistic validation presented here underscores the enduring value of the ethnopharmacological approach to in drug discovery.

PMID 41931959
Read full article →
PubMedCell2026-03-21

Hijacking ERAD for targeted degradation of transmembrane proteins.

Song Haikun H, Wang Wei W, Mei Tingfang T, Zheng Huiwen H et al.

Targeted protein degradation (TPD) technologies provide huge opportunities for drug discovery, but degrading transmembrane (TM) targets remains challenging. Since TM proteins are canonically folded on the endoplasmic reticulum (ER) membrane, we hypothesized that harnessing ER-associated degradation (ERAD) may enable efficient degradation of TM proteins. Here, we established a TPD technology hijacking ERAD and named it ERAD-engaging chimeras (ERADECs), capable of degrading TM targets with high efficacy. We identified desonide as a binder of SYVN1, an ER E3 ligase mediating ERAD. We designed ERADECs targeting programmed death-ligand 1 (PD-L1) by connecting desonide to a known PD-L1 ligand and observed SYVN1- and ERAD-dependent PD-L1 degradation with high efficacy. Functionally, these ERADECs exhibited stronger tumor suppression and PD-L1-lowering effects than a clinically used PD-L1 antibody in vivo. The concept of ERADECs is also expandable to other membrane targets. Collectively, we established a platform technology hijacking ERAD to selectively degrade TM targets with remarkable efficiency.

PMID 41861782
Read full article →
PubMedArchiv der Pharmazie2026-02-19

Investigating the Telomerase Downregulatory Potential of Steroidal Drugs Following Pharmacophore-Based Rational; Computational and In Vitro Assessments.

Al-Karmalawy Ahmed A AA, Alabdali Aya Yaseen Mahmood AYM, Yousef Tarek A TA, Elmaaty Ayman Abo AA et al.

Inhibiting telomerase could lead to telomere shortening, chromosomal instability, and eventually cell death in cancer cells. The use of steroids in cancer treatment is significant; besides, drug repurposing can be a quicker and less expensive method of drug discovery than de novo drug development. Accordingly, diverse 280 steroidal drugs-following a pharmacophore-based rationale-were docked against telomerase receptor and compared to the co-crystallized inhibitor (BIBR1532) as a reference standard. Additionally, a molecular dynamics simulation for 200 ns was performed to confirm the docking results. Moreover, the six steroidal drugs (Betamethasone disproportionate, Beclomethasone disproportionate, Clobetasone butyrate, Desonide, diflucortolone valerate, and Hydrocortisone butyrate) were selected for further in vitro investigation. The antitumor activities of the six steroidal drugs against H1299, HuH7, HCT116, A549, MDA-MB-231, MCF7, PC3, MG63, and A375 cancer cell lines, besides OEC and HSF normal cell lines, were evaluated and compared to doxorubicin (Dox) as a reference positive standard. Especially, Clobetasone butyrate represented the better cytotoxicity against seven cancer cell lines (H1299, HuH7, HCT116, MDA-MB-231, PC3, MG63, and A375) with IC50 values of 12.56, 13.95, 12.00, 17.51, 11.69, 20.64, and 20.21 µg/mL, respectively. The outstanding antitumor six steroidal drugs were further investigated for their telomerase downregulatory potentials. All analogs recorded outstanding downregulatory results against telomerase, especially Clobetasone butyrate, Desonide, Diflucortolone valerate, and Hydrocortisone butyrate, where the protein expression for telomerase was downregulated up to 0.66-, 0.76-, 0.56-, and 0.73-fold change for clobetasone butyrate, desonide, diflucortolone valerate, and hydrocortisone butyrate, respectively, compared to the control.

PMID 41709500
Read full article →
PubMedLasers in surgery and medicine2026-01-29

Hydroxybutyl Chitosan Hydrogel Promotes Ablative Fractional CO2 Laser Wound Healing: A Prospective, Randomized, Split-Face Trial and Animal Model Evidence.

Wu Haien H, Huang Wenyue W, Cai Xinze X, He Hailun H et al.

Although effective for atrophic acne scars, ablative fractional CO₂ laser (AFCL) causes unavoidable downtime and carries the potential for post-inflammatory hyperpigmentation (PIH). To evaluate the efficacy and safety of hydroxybutyl chitosan (HBC) in wound healing and to investigate the possible molecular mechanisms of HBC. Eighteen participants were enrolled in a split-face study, with each hemiface randomly assigned to receive either HBC or positive control therapy (PC: desonide cream, epidermal growth factor gel, and fusidic acid cream in combination) following AFCL. Clinical assessments included erythema, edema, pain, the time to decrustation, the skin barrier function, and melanin were assessed. In parallel, a mouse skin wound healing model was employed to investigate the effects of HBC. The expression of interferon regulatory factor 7 (IRF7) and cathepsin S (Ctss), as well as M1 and M2 macrophage polarization, was evaluated by immunohistochemistry and Western blot analysis of mouse skin tissues. Although HBC exhibited a slightly delayed onset of wound healing compared to the PC protocol, it achieved comparable outcomes by Days 7 and 28 between the groups. HBC showed more early pain but no steroid-related irritation and better moisturization. In mice, HBC demonstrated effects comparable to PC drugs, promoting macrophage M2 polarization and upregulating IRF7 and Ctss expression. HBC is effective and safe for promoting wound healing post AFCL. HBC upregulates IRF7 and Ctss expression and promotes macrophage M2 polarization. The expression of IRF7/CTSS may be correlated with M2 polarization of macrophages. ChiCTR2200063765.

PMID 41607028
Read full article →
PubMedDermatitis : contact, atopic, occupational, drug2025-10-14

Letter: The Paradox of Desonide: Treating Inflammation, Triggering Allergy.

Ben Salah Nesrine N, Ben Yahia Mounira M, Belhadjali Hichem H, Ben Belgacem Manel M et al.

PMID 41084299
Read full article →

+122 more articles available with a free account

Sign up free to view all articles →

Ask about desonide