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Oncology · Clinical trials

Basal Cell Carcinoma Clinical Trials

Approved therapies, the pivotal-trial endpoints they were judged on, the magnitude of benefit — and the drugs that failed their endpoints, and why.

Indication overview

About basal cell carcinoma — and why its trials are hard

Basal cell carcinoma is the most common human cancer, a slow-growing keratinocyte malignancy of the skin driven overwhelmingly by aberrant Hedgehog signalling, most often through inactivating PTCH1 mutations or activating SMO mutations. The vast majority of cases are cured by simple surgical excision, Mohs micrographic surgery, or local destructive/topical therapies, and metastasis is rare. Systemic therapy is reserved for the small minority with locally advanced disease not amenable to surgery or radiotherapy, or with metastatic disease. For these patients the Hedgehog pathway inhibitors vismodegib and sonidegib, which block the smoothened (SMO) receptor, produce meaningful response rates and were practice-changing. Their use is limited by characteristic on-target toxicities (muscle spasms, dysgeusia, alopecia) causing frequent discontinuation, and by acquired resistance. For patients who progress on or cannot tolerate Hedgehog inhibitors, the anti-PD-1 antibody cemiplimab provides an immunotherapy option, exploiting the very high ultraviolet-induced mutational burden of these tumours. Overall prognosis for advanced BCC has improved markedly, though durable control after Hedgehog-inhibitor failure remains an area of need.

Indication
Basal Cell Carcinoma
ICD-10-CM
C44.91 — Basal cell carcinoma of skin

Approved therapies & pivotal evidence

What's been approved — and by how much it moved the endpoint

Drug (brand)ApprovedSettingPivotal trialPrimary endpointMagnitude of benefit
Vismodegib (Erivedge)2012Metastatic BCC, or locally advanced BCC recurring after surgery or unsuitable for surgery/radiotherapyERIVANCE (phase 2)Objective response rateORR ~43% in locally advanced and ~30% in metastatic BCC
Sonidegib (Odomzo)2015Locally advanced BCC recurring after surgery/radiotherapy or unsuitable for themBOLT (phase 2)Objective response rateORR ~56% in locally advanced BCC (investigator-assessed); durable responses
Cemiplimab (Libtayo)2021Locally advanced (accelerated) or metastatic BCC after Hedgehog inhibitor or when a HHI is not appropriateStudy 1620 (phase 2)Objective response rateORR ~31% in locally advanced BCC after HHI therapy, with durable responses

Choosing the right endpoint

Primary endpoints that matter in basal cell carcinoma trials

  • Objective response rate (ORR) — Primary endpoint for all advanced-BCC approvals (ERIVANCE, BOLT, cemiplimab), reflecting rarity of advanced disease and single-arm designs
  • Duration of response (DoR) — Critical secondary measure given on-target Hedgehog toxicities and acquired resistance limiting long-term benefit
  • Progression-free survival (PFS) — Supportive endpoint in single-arm trials of advanced disease
  • Complete response rate — Meaningful in locally advanced disease where complete clearance can restore surgical resectability
  • Safety/tolerability and discontinuation rate — Especially important for Hedgehog inhibitors, where muscle spasms, dysgeusia and alopecia drive frequent treatment interruption

How iNGENū runs basal cell carcinoma trials

Physician-led design, built for FDA submission

Endpoint & biomarker strategy

Board-certified specialists design endpoints and patient selection aligned to current FDA guidance for this indication.

FDA-ready data

Built to ICH-GCP and 21 CFR 312.120, with direct FDA submission — data accepted by the FDA, EMA and MHRA.

Faster, lower-cost delivery

~4-week ethics via the TGA CTN scheme, up to 43.5% R&D rebate, and 80–90% below US CRO cost.

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Frequently asked questions

Basal Cell Carcinoma clinical trials — FAQs

Does most basal cell carcinoma need systemic drugs?
No. The overwhelming majority of BCCs are cured by surgery (including Mohs), radiotherapy, or local/topical treatments, and rarely spread. Systemic therapy is reserved for the small subset with locally advanced tumours unsuitable for those options, or metastatic disease.
How do Hedgehog inhibitors work?
BCC is driven by inappropriate Hedgehog pathway activation. Vismodegib and sonidegib block the smoothened (SMO) receptor, switching off this signalling. They shrink tumours in many patients but often cause muscle cramps, taste changes and hair loss that limit tolerability.
What can be done after Hedgehog inhibitors stop working?
Tumours can acquire resistance or patients may not tolerate these drugs. Cemiplimab, a PD-1 immunotherapy approved in 2021, offers an alternative that harnesses the immune system against these highly UV-mutated tumours, providing durable responses in some patients.

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