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Tirbanibulin — SCE Dermatology MCQ

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HardSkin CancerTirbanibulinSCE Dermatology

A 60-year-old man has chronic plaque psoriasis and has been prescribed Tirbanibulin 1% ointment for actinic keratoses on his face. What is the mechanism of Tirbanibulin?

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Correct answer: BDual inhibitor of Src kinase and tubulin polymerisation — causes antiproliferative and pro-apoptotic effects on dysplastic keratinocytes

The correct answer is B, dual inhibitor of Src kinase and tubulin polymerisation, causing antiproliferative and pro-apoptotic effects on dysplastic keratinocytes. Tirbanibulin 1% ointment is licensed for field treatment of actinic keratoses of the face and scalp, and its mechanism combines inhibition of Src kinase signalling (which reduces proliferative and migratory signalling in dysplastic keratinocytes) with disruption of microtubule assembly, arresting the cell cycle and triggering apoptosis selectively in rapidly dividing dysplastic cells. This dual action distinguishes it from other topical AK therapies and underpins its short, 5-day once-daily application course, which is far shorter than 5-fluorouracil or imiquimod regimens. The stem's clue of a psoriasis patient being prescribed a novel AK ointment tests recognition of this specific, exam-relevant mechanism rather than more familiar biologic or pathway inhibitors used in psoriasis itself. Why the other options are wrong: C. EGFR inhibitor: this describes agents like cetuximab or panitumumab used in oncology, not a mechanism attributed to tirbanibulin, which acts on Src kinase and tubulin, not the epidermal growth factor receptor pathway. D. Hedgehog pathway inhibitor: this describes vismodegib and sonidegib, used systemically for advanced basal cell carcinoma via smoothened receptor blockade, an entirely different target and indication to topical AK treatment. E. IL-17 inhibitor: this describes biologics such as secukinumab or ixekizumab used for moderate to severe plaque psoriasis, relevant to this patient's psoriasis but not to the actinic keratosis treatment being asked about. A. PDE4 inhibitor: this describes apremilast (oral, psoriasis/psoriatic arthritis) and crisaborole; tirbanibulin has no phosphodiesterase-4 inhibitory activity. Key point: Tirbanibulin's unique dual Src kinase and tubulin polymerisation inhibition drives its short 5-day course and selective pro-apoptotic effect on dysplastic keratinocytes in actinic keratosis.

Reference: electronic Medicines Compendium (emc), Klisyri 1% ointment (tirbanibulin) Summary of Product Characteristics, section 5.1 Pharmacodynamic properties, 2023, https://www.medicines.org.uk/emc/product/13111