Acne pathology

The first and only topical androgen-receptor inhibitor that reduces sebum production1

Pathophysiology in acne vulgaris

Acne pathology is characterized by four key elements.

The pathophysiology of acne is multifactorial and involves four key, interrelated factors: inflammation, follicular hyperkeratinization, increased sebaceous gland activity and sebum production, and colonization by Cutbacterium acnes (formerly Propionibacterium acnes).11

Androgen-mediated excess sebum production is implicated as an early step in acne vulgaris pathophysiology and is therefore considered an important therapeutic target.12 Evidence indicates that excess sebum production is an important driver in acne pathogenesis as it promotes growth, reproduction, and accumulation of skin cells in the hair follicle. Furthermore, it provides an anaerobic environment that facilitates C. Acne proliferation and therefore inflammation. Androgens can also directly induce expression of inflammatory cytokines.11

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Acne and the PILOSEBACEOUS UNIT

Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit comprising the hair follicle hair shaft and sebaceous gland.13,14

pilosebaceous unit

Topical treatments and their specific therapeutic target

WINLEVI® is the first and only topical that targets sebum production – and thus intervenes early in the first step of the acne cascade.1

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Indication

WINLEVI® (clascoterone) 10 mg/g cream is indicated for the topical treatment of acne vulgaris in patients 12 years of age and older.2

Adverse event reporting

Adverse events should be reported. Reporting forms and information can be found at yellowcard.mhra.gov.uk. Adverse events should also be reported to Glenmark Pharmaceuticals Europe Ltd medical_information@glenmarkpharma.com or call 0800 458 0383.

References

  1. Rosette C, et al. J Drugs Dermatol. 2019;18(5):412-418.
  2. WINLEVI® SPC.
  3. Eichenfield LF, et al. J Drugs Dermatol. 2024;23(1):1278-1283.
  4. Purdy S, DeBerker D. BMJ Clin Evid. 2008;1714.
  5. Zouboulis CC, Bettoli V. Br J Dermatol. 2015;Suppl 1:27-36.
  6. ONS. Estimates of the population for the UK, England, Wales, Scotland and Northern Ireland. Accessed 27 June 2024. https://www.ons.gov.uk/peoplepopulationandcommunity/populationandmigration/populationestimates/datasets/populationestimatesforukenglandandwalesscotlandandnorthernireland.
  7. Primary Care Dermatology Society. Acne: acne vulgaris. Accessed 27 June 2024. https://www.pcds.org.uk/clinical-guidance/acne-vulgaris.
  8. Dawson AL, et al. BMJ. 2013;346:f2634.
  9. Layton AM, Thiboutot D, Tan J. Br J Dermatol. 2021;184(2):219-225.
  10. Morshed ASM, et al. Sci Rep. 2023; 13: 21084.
  11. Baldwin, H et al. J Drugs Dermatol. 2023;22(6):582-587.
  12. Del Rosso JQ, Kircik L. J Dermatolog Treat. 2024;35(1):2298878.
  13. Kurokawa I, et al. Dermatol Ther (Heidelb). 2021;11(4):1129-1139.
  14. Tuchayi S, et al. Acne vulgaris. Nat Rev Dis Primers. 2015; 1:15029.
  15. Kim HJ, et al. Int J Mol Sci. 2024;25(10):5302.
  16. Hebert A, et al. J Drugs Dermatol. 2023;22(2):174-181.
  17. Hebert A, et al. JAMA Dermatol. 2020;156(6):621-630.
  18. Abelson MB, Fink K. (2003). Controlling for the Placebo Effect. Review of Ophthalmology. Accessed October 2024.
  19. Hebert A, et al. JAMA Dermatology. 2020;156(6):621-630 (Supplement 1).
  20. Eichenfield L, et al. J Am Acad Dermatol. 2020;83(2):477-485.
  21. Mazzetti A, et al. J Drugs Dermatol. 2019;18(6):563.
  22. NICE Clinical Knowledge Summary. Acne vulgaris.

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