Final results of a multicenter phase II study of the purine nucleoside phosphorylase (PNP) inhibitor forodesine in patients with advanced cutaneous t-cell lymphomas (CTCL) (Mycosis fungoides and Sézary syndrome)

Abstract

Oral forodesine at a dose of 200 mg daily is feasible and shows partial efficacy in this highly selected CTCL population and some durable responses.

Lack of durable disease control with chemotherapy for mycosis fungoides and Sézary syndrome: a comparative study of systemic therapy

“…Adverse effects, particularly the risk of infection, vary greatly with each therapy. Drugs such as forodesine have known T-cell effects, 55 but even novel agents can increase the risk of infection. [56][57][58] Data on adverse events was not available for this patient cohort, but it remains important for the clinician to consider the balance of these in guiding management decisions.…”

Long‐term efficacy and safety of bexarotene for Japanese patients with cutaneous T‐cell lymphoma: The results of a phase 2 study (B‐1201)

“…Patients with advanced‐stage CTCL may require various combinations, mainly including radiation therapy, biological response modifiers and chemotherapy. Recent advances in elucidating biophysiological characteristics or novel molecular targets on CTCL have promoted new therapeutic modalities such as histone deacetylase inhibitors, molecular‐targeted agents and purine nucleoside phosphorylase inhibitors …”

Other Chemotherapeutic Agents in Cutaneous T-Cell Lymphoma

“…The median duration of response was 127 days. Dummer and colleagues 129 recently published a phase II multicenter study of forodesine in 144 individuals, in whom 101 patients with stage IIB or greater disease were assessed for efficacy of the drug. Patients were administered 200 mg orally daily (approximately equivalent to 80 mg/m 2 ).…”

“…Side effects include nausea, fatigue, reversible lymphopenia, and cutaneous infections. 127,129 PROTEASOME INHIBITORS: BORTEZOMIB Bortezomib (Velcade) is a cell-permeable dipeptide boronic acid that reversibly inhibits the b5 subunit of the proteasome. Multiple prooncogenic factors are under proteasome control, such as transcription factors, cyclins, cyclindependent kinase inhibitors, and apoptotic factors.…”