calcipotriol / Generic mfg. - LARVOL DELTA

Topical sulforaphane exacerbates disease and promotes the accumulation of inflammatory CD8+ T cells in a dermatitis model. (PubMed, bioRxiv) - "Topical SFN worsens MC903-induced dermatitis through a mechanism involving the peripheral accumulation of IFNγ-producing CD8 + T cells in skin. These findings demonstrate that SFN can exert context-dependent pro-inflammatory effects and underscore the need to evaluate its effects carefully when considering topical medical or cosmetic applications."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Dermatopathology • Immunology • Inflammation • CD4 • CD8 • IFNG • TRB

Age-related changes of FCGR3A+ natural killer cells and their association with elderly atopic dermatitis. (PubMed, EBioMedicine) - "In conclusion, NK cells, especially the NK2 subset, are associated with AD pathogenesis, with potential implications for elderly patients."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • CXCL12 • CXCL14 • FCGR3A

Type 3 Inflammation-Specific Keratinocyte Glutaminolysis Promotes Skin Inflammation. (PubMed, JCI Insight) - "Amino acid or antioxidant supplementation partially rescued these defects, whereas rapamycin blocked the amino acid-mediated proliferative rescue. Gls1 deletion did not impair steady-state skin development or homeostasis and did not alter MC903-induced type 2 dermatitis, but it delayed wound re-epithelialization and attenuated IMQ-induced psoriasiform inflammation. Loss of keratinocyte GLS1 also reduced epidermal chemokine expression and the accumulation of neutrophils and IL-17A-producing γδ T cells, revealing a role for glutaminolysis in amplifying epithelial-immune crosstalk. These findings define GLS1-mediated glutaminolysis as a context-specific metabolic checkpoint linking type 3 inflammation to keratinocyte proliferation and cutaneous immune amplification, and support locally or temporally controlled GLS1 inhibition as a potential therapeutic strategy for psoriasis."

Journal • Dermatitis • Dermatology • Immunology • Inflammation • Psoriasis • GLS1 • IL17A

Disease Progression-dependent Neurobehavioral Phenotypes of Agitation, Anxiety, and Depression in MC903-induced Chronic Itch. (PubMed, J Invest Dermatol) - "Female mice exhibited accelerated and more severe emotional disturbances under conditions producing only mild agitation in males. This study identifies itch-induced agitation, describes a time-, dose-, and sex-dependent emotional progression, and establishes NAc and CeA as causal neural substrates, suggesting specific targets for therapeutic intervention in chronic itch-associated psychiatric comorbidities."

Journal • CNS Disorders • Depression • Dermatology • Mood Disorders • Pruritus • Psychiatry • FOS

Shared Treg dysregulation underlies psoriasis vulgaris and atopic dermatitis through the PHF19-PRC2 epigenetic axis. (PubMed, Front Immunol) - "Findings were validated in Foxp3-tdTomato reporter mouse models of imiquimod-induced psoriasis-like and MC903-induced AD-like dermatitis by flow cytometry and quantitative PCR. Molecular docking and in vivo experiments demonstrated that resveratrol binds PHF19, is predicted to activate the PHF19-PRC2-H3K27me3 axis, restores Treg subset homeostasis, and ameliorates skin lesions in both models. Treg subset remodeling is a shared pathogenic feature, nominating PHF19-targeted activation as a tolerance-restoring therapeutic strategy."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • Psoriasis • CD74 • CXCR4 • FOXP3 • GNAQ

Jiu-Wei-Yong-An decoction alleviates atopic dermatitis by suppressing TLR4/MyD88/NF-κB signaling pathway. (PubMed, J Ethnopharmacol) - "JWYA ameliorates AD through multi-component, multi-target modulation of the TLR4/MyD88/NF-κB inflammatory axis. Phylliroside and Suspenoidside B are key bioactive substances that directly bind TLR4/MyD88/NF-κB to inhibit NF-κB hyperactivation, relieving AD-related inflammation. This study provides experimental basis for JWYA's clinical application and subsequent monomer drug development."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • IFNG • MYD88 • TLR4 • TNFA

Construction of a butyrate-producing engineered bacteria and its therapeutic effects on atopic dermatitis (PubMed, Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi) - "This study aims to construct an engineered Escherichia coli Nissle 1917 (EcN) strain capable of efficient and stable butyrate secretion, and evaluate its therapeutic efficacy in a calcipotriol (MC903)-induced mouse model of AD...Furthermore, EcN-But treatment significantly downregulated serum total IgE levels and suppressed the expression of key inflammatory cytokines in skin tissues. Conclusion The engineered strain EcN-But effectively alleviates AD-like inflammation by enabling in situ butyrate secretion in the gut to modulate systemic immune homeostasis, offering a novel live biotherapeutic product strategy for the clinical management of atopic dermatitis."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Oncology • IL13 • IL33 • IL4 • TNFA • TSLP

GALNT6-mediated O-glycosylation suppresses NLRP3 inflammasome activation to alleviate atopic dermatitis. (PubMed, Life Sci) - "GALNT6 may function as a compensatory protective regulator of cutaneous inflammation by modulating NLRP3 O-glycosylation and inflammasome activation. These findings identify the GALNT6-NLRP3 pathway as a potential target for further mechanistic and therapeutic investigation in AD."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • IL1B • NLRP3

Topical Application of Indole-3-Acetic Acid, Present in S. epidermidis Supernatant, Alleviates Atopic Dermatitis in Mice at Least via the Aryl Hydrocarbon Receptor Signalling Pathway. (PubMed, Exp Dermatol) - "In an MC903-induced AD-like mouse model, cutaneous IAA levels and S. epidermidis abundance were reduced...Molecular docking predicted a possible interaction between IAA and AHR, and in vitro assays showed that IAA modulated keratinocyte AHR-associated inflammatory and barrier-related responses. Together, our findings support IAA as a microbiome-associated postbiotic candidate for AD management, at least partly through AHR-associated signalling."

Journal • Preclinical • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Infectious Disease • Inflammation

Topical exposure to di(2-ethylhexyl) phthalate aggravates atopic dermatitis: an integrated network toxicology, bioinformatics, and experiment analysis. (PubMed, Food Chem Toxicol) - "Importantly, in vivo experiments demonstrated that topical DEHP exposure exacerbates MC903-induced AD-like dermatitis in BALB/c mice...Finally, molecular docking suggested potential binding modes between DEHP and these proteins, providing structural hypotheses for their possible involvement in this process. Together, our findings indicate that cutaneous DEHP exposure may exacerbate AD by promoting endothelial adhesion and immune-cell infiltration, thereby intensifying skin inflammation."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • CXCR1 • SELP

Targeting TRPV4 with sclareol ameliorates atopic dermatitis through by suppression of inflammatory response and oxidative stress. (PubMed, Biochem Pharmacol) - "With an MC903‑induced AD mouse model, we found that sclareol treatment significantly alleviated skin lesions, reduced epidermal thickening, decreased infiltration of CD4+ T cells, and lowered serum levels of immunoglobulin E (IgE), interleukin (IL)-1β, and IL-13...To confirm target specificity, we used TRPV4‑knockout cells; notably, observed anti‑inflammatory and antioxidant effects were substantially attenuated in the absence of TRPV4. Collectively, this study establishes sclareol as a novel TRPV4 inhibitor that ameliorates AD pathology through a TRPV4‑dependent mechanism involving suppression of inflammatory signaling and oxidative stress."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • Oncology • CD4 • IL13 • TNFA

MDI1228, a topical pan-JAK inhibitor, disrupts dermal fibroblast-T cell chemokine crosstalk to resolve allergic contact and atopic dermatitis. (PubMed, Front Immunol) - "MDI1228 was evaluated in DNFB‑induced ACD and MC903‑induced AD mouse models, as well as in primary mouse and human cell‑based assays...Compared with glucocorticoids, prolonged topical application of MDI1228 showed minimal systemic toxicity and preserved tissue homeostasis. These findings identify dFBs as a central therapeutic node and demonstrate that MDI1228, by directly targeting T cells and disrupting dFB‑derived chemokine axes via JAK inhibition, offers a potent and safe topical treatment for both ACD and AD."

Journal • Atopic Dermatitis • Contact Dermatitis • Dermatitis • Dermatology • Immunology • CCL2 • CCR2 • CXCL9 • CXCR3 • JAK1 • JAK2 • TYK2

Panax notoginseng extract alleviates atopic dermatitis-like skin inflammation associated with suppression of the cGAS-STING pathway. (PubMed, Front Pharmacol) - "The anti-AD effects of PNE were evaluated in both an AD-like mouse model induced by calcipotriol (MC903) and a human keratinocyte (HaCaT) cell model stimulated with tumor necrosis factor-alpha and interferon-gamma (TNF-α/IFN-γ)...PNE exerts anti-AD effects by attenuating Th2-mediated inflammatory responses via modulation of the cGAS-STING pathway. These findings suggest that PNE has the potential to serve as a natural therapeutic option for AD."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • Metabolic Disorders • Oncology • Pruritus • CCL2 • CCL22 • CCL5 • CGAS • IFNG • IL13 • IL4 • IRF7 • TNFA

Effects of electroacupuncture at "Hegu" (LI4) and "Quchi" (LI11) on Parthanatos in atopic dermatitis mice by regulating the PAR2/TRPV3 pathway (PubMed, Zhen Ci Yan Jiu) - "EA at LI4 and LI11 can alleviate skin inflammatory injury and itching in AD mice, and its mechanism may be related to down-regulating the PAR2/TRPV3 pathway and inhibiting Parthanatos in skin cells."

Journal • Preclinical • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • AIF1 • IL13 • IL33 • MIF • PARP1 • TRPV3

Anti-Inflammatory and Barrier-Related Effects of Bidens bipinnata L. Fruit Ethanol Extract in an MC903-Induced AD-like Dermatitis Mouse Model and LPS-Stimulated RAW 264.7 Cells. (PubMed, Int J Mol Sci) - "Notably, EEBB significantly improved skin hydration-related parameters, including relative skin hydration readings and the post-application moisture retention profile, and partially restored filaggrin and loricrin expression in lesional skin, whereas dexamethasone showed limited effects on these hydration-related parameters under the present conditions. These effects were associated with inhibited phosphorylation of JNK and p38 MAPK, with no marked effect on ERK phosphorylation under the present conditions. In conclusion, EEBB effectively alleviated AD-like dermatitis, accompanied by improved skin hydration and restoration of barrier-related protein expression, attenuation of local inflammatory responses, and targeted inhibition of the MAPK signaling pathway."

Journal • Preclinical • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • FLG • IFNG • IL4 • IL5 • LORICRIN • PTGS2 • TNFA

Cross-species transcriptomic evidence for peripheral-central immune crosstalk in atopic dermatitis. (PubMed, Front Immunol) - "We integrated neuroimaging transcriptomics based on resting-state functional MRI data from AD patients (n=19) and healthy controls (n=36) with transcriptomic profiling and experimental validation in MC903-induced AD mouse models...These findings suggest that chronic peripheral inflammation may be associated with neuroinflammation and neurotransmitter imbalance centered in the LSFG and prefrontal cortex, contributing to specific brain activation patterns in AD patients. This study uncovers a novel peripheral-central immune interaction mechanism in AD and provides new insights for developing neuroimmune-targeted therapeutic strategies."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • Pruritus • AIF1 • CXCL10 • GFAP • IL33 • IL6

Single-cell transcriptomic analysis identifies a MIF-driven keratinocyte-macrophage-Th2 axis as a key inflammatory circuit in atopic dermatitis. (PubMed, Inflamm Res) - "Our findings identify a critical role for the MIF signaling axis in mediating crosstalk between proliferative keratinocytes and M2-polarized macrophages, thereby promoting Th2-driven inflammation in AD. Targeting MIF may represent a potential therapeutic strategy for AD."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • CCL2 • CCL22 • CD74 • IL10 • IL13 • MIF • MRC1 • PTPRC • TERC

High-salt diet promotes atopic dermatitis by partially enhancing intestinal SGK1/ENaC signaling and destroying gut Lactobacillus-maintained systemic type 1 interferon. (PubMed, Front Cell Infect Microbiol) - "MC903 was applied topically to establish AD in wild-type C57BL/6 mice; in mice with IFN1 receptor-1 (ifnar1) knockout, sgk1 conditional knockout (cKO) in intestinal epithelial cells (IECs), or stimulator of interferon genes (sting) cKO in dendritic cells (DCs); and in BDCA2-DTR mice with plasmacytoid DC (pDC) deletion...HSD promotes AD by partially impairing the systemic IFN1 production that is orchestrated by STING signaling in DCs by reducing the gut Lactobacillus and by partially increasing the sodium accumulation in skin lesions via driving the ileum SGK1 phosphorylation and βENaC and γENaC expression. Further research is necessary to assess the effect of Lactobacillus supplementation on clinical AD patients with an HSD habit."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • IFNAR1 • IL13 • IL4 • STING • TJP1

Plasmacytoid dendritic cells alleviate atopic dermatitis by suppressing Th2 inflammation via the IFN-α/IFNAR1 pathway. (PubMed, Front Immunol) - "We employed an integrative approach combining transcriptomic analysis, flow cytometry, an MC903-induced murine model of AD, in vivo expansion of pDCs using FLT3L, targeted depletion of pDCs with the 120G8 antibody, and IFNAR1-deficient mice...We show that pDCs negatively regulate Th2 inflammation and maintain barrier integrity via the IFN-α/IFNAR1 pathway. These findings provide a theoretical and experimental foundation for targeting pDCs and their downstream signaling as a novel therapeutic strategy in AD."

Journal • Asthma • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • Pruritus • Pulmonary Disease • Respiratory Diseases • IFNA1 • IFNAR1 • IL13 • IL4

Early Pregnancy Exposure to Organophosphate Esters and Risk of Infant Atopic Dermatitis: Sex-Specific Association Analyses in a Community-Based Birth Cohort. (PubMed, Environ Pollut) - "This study provides evidence that early gestational exposure to TDBPP is associated with increased infant AD risk. Exploratory analyses suggest sex-specific effects. We also established an animal model and identified mechanistic pathways for future research."

Journal • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Oncology • TNFA

Automated 24-Hour Quantification of Scratching Behavior Reveals Distinct Physiological and Allergic Pruritus Signatures in Mice (EAACI 2026) - "In contrast, induction of allergic dermatitis using MC903 or 2,4-dinitrofluorobenzene (DNFB) caused a robust and sustained increase in scratching behavior that persisted for more than 36 hours...Conclusion In summary, we developed a practical and reliable system SHIGUSA for long-term automated scratching analysis and demonstrated distinct temporal and structural features of physiological and pathological pruritus in mice. This approach enables unbiased detection of subtle and chronic scratching phenotypes that have remained inaccessible with conventional observation-based methods and provides a powerful tool for mechanistic and therapeutic studies of pruritus."

Preclinical • Dermatitis • Immunology • Inflammation

The role of B cells in allergic contact dermatitis and in tolerance to contact allergens (EAACI 2026) - "A complementary mouse study used a PPD-induced ACD model, with or without PPD tolerance induction with the Vitamin D analog (MC903) and included B-cell–depleted mice to evaluate MC903-induced tolerance, dermal B-cell infiltration and B-cell responses to PPD in secondary lymphoid organs...Conclusion These findings challenge the view of the skin as a B cell independent organ and suggest that B cells contribute to the balance between inflammation and tolerance to contact allergens. Defining their transcriptional and functional programs may reveal mechanisms of allergen tolerance, identify targets for mechanism-based therapies for ACD and suggest that altered B-cell responses may also be relevant for other inflammatory skin diseases."

Dermatitis • Immunology

Lindera obtusiloba extract attenuates cytokine-mediated epidermal inflammation in keratinocytes and an MC903-induced AD-like mouse model. (PubMed, Sci Rep) - "In the co-culture model, LM reduced inflammatory gene expression in THP-1 cells. Collectively, these findings indicate that LM suppresses keratinocyte-derived inflammatory mediator production and ameliorates MC903-induced AD-like epidermal inflammation, supporting its potential as a lignan-enriched anti-inflammatory fraction for AD-associated cutaneous inflammation."

Journal • Preclinical • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • CD4 • CXCL8 • IFNG • TNFA • TSLP

Intralesional 5-Fluorouracil (5FU), Topical Calcipotriene Treatment for SCC (clinicaltrials.gov) - P1 | N=30 | Recruiting | Sponsor: Melissa Pugliano-Mauro | Trial completion date: Oct 2026 ➔ Oct 2027 | Trial primary completion date: Sep 2026 ➔ Sep 2027

Trial completion date • Trial primary completion date • Oncology • Squamous Cell Carcinoma

Genistein alleviates skin inflammation in atopic dermatitis by inhibiting mast cell degranulation through toll-like receptor. (PubMed, Phytomedicine) - "Our findings demonstrate that genistein alleviates AD by specifically targeting the D127 and R226 sites of TRAM to inhibit mast cell activation via the PLCγ1-IKKβ-NF-κB pathway. This work elucidates a novel pharmacological mechanism of a natural compound and identifies TRAM as a promising new therapeutic target for allergic inflammatory diseases, highlighting the value of natural products in developing targeted immunomodulatory therapies."

Journal • Allergy • Atopic Dermatitis • Dermatitis • Dermatology • Immunology • Inflammation • IL4 • TNFA