# Therapeutic potential of Licochalcone A in dermatological diseases: from basic to clinical research

**Authors:** Deming Liu, Xue Jiang, Fujin Yang, Jingjing Zhou, Yanxi Li, Hua Yang

PMC · DOI: 10.3389/fphar.2025.1632006 · Frontiers in Pharmacology · 2025-10-16

## TL;DR

Licochalcone A, a natural compound, shows promise in treating various skin conditions by targeting multiple biological pathways.

## Contribution

This review highlights Lico-A's therapeutic potential and mechanisms in dermatology, identifying research gaps and future directions.

## Key findings

- Lico-A targets pathways like NLRP3, NF-κB, and Nrf2/HO-1 to modulate inflammation and oxidative stress.
- Clinical studies confirm Lico-A's efficacy in reducing skin lesions and improving barrier function.
- Current limitations include lack of high-quality trials and geographic bias in research.

## Abstract

Licochalcone A (Lico-A), a flavonoid compound extracted from Glycyrrhiza uralensis, exhibiting multiple pharmacological properties including anti-inflammatory, antibacterial, antioxidant, and antitumor effects. It demonstrates significant therapeutic potential in the field of dermatological treatment. This review focuses on the efficacy of Lico-A in the treatment of acne, atopic dermatitis, rosacea, pigmentation disorders, and skin tumors. Mechanistically, Lico-A targets multiple signaling pathways such as NLRP3 inflammasome, NF-κB, PLC/ERK/STAT3, AP-1, and Nrf2/HO-1, thereby modulating inflammatory cascades, oxidative stress, melanogenesis, and tumorigenic processes. Clinical studies have also confirmed its ability to reduce inflammatory lesions, improve skin barrier function, and suppressing hyperpigmentation. However, current research is limited by geographical bias, a lack of high-quality randomized controlled trials, and reliance on preclinical models. Future studies should focus on multicenter randomized controlled trials, advanced delivery systems, and mechanistic investigations using systems biology. Addressing these gaps could establish Lico-A as a multifunctional, evidence-based dermatologic therapy for inflammatory, infectious, and neoplastic skin disorders.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], FOS (Fos proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2353]
- **Chemicals:** Licochalcone A (PubChem CID 5318998)
- **Diseases:** acne (MONDO:0011438), atopic dermatitis (MONDO:0004980), rosacea (MONDO:0006604)
- **Species:** Glycyrrhiza uralensis (taxon 74613)

## Full-text entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}, FOSB (FosB proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 2354] {aka AP-1, G0S3, GOS3, GOSB}, HSPG2 (heparan sulfate proteoglycan 2) [NCBI Gene 3339] {aka HSPG, PLC, PRCAN, SJA, SJS, SJS1}, MAPK1 (mitogen-activated protein kinase 1) [NCBI Gene 5594] {aka ERK, ERK-2, ERK2, ERT1, MAPK2, NS13}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, HMOX1 (heme oxygenase 1) [NCBI Gene 3162] {aka HMOX1D, HO-1, HSP32, bK286B10}
- **Diseases:** tumorigenic (MESH:D002471), acne (MESH:D000152), hyperpigmentation (MESH:D017495), atopic dermatitis (MESH:D003876), inflammatory, infectious, and neoplastic skin disorders (MESH:D012874), pigmentation disorders (MESH:D010859), dermatological diseases (MESH:D000168), rosacea (MESH:D012393), skin tumors (MESH:D012878), inflammatory (MESH:D007249)
- **Chemicals:** Lico-A (MESH:C070840), flavonoid (MESH:D005419)
- **Species:** Glycyrrhiza uralensis (Chinese licorice, species) [taxon 74613]

## Full text

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## Figures

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## References

56 references — full list in the complete paper: https://tomesphere.com/paper/PMC12571894/full.md

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Source: https://tomesphere.com/paper/PMC12571894