Inhibition of metastasis in a castration resistant prostate cancer model by the quinoline‐3‐carboxamide tasquinimod (ABR‐215050)

Abstract

In conclusion, this study and clinical data show that tasquinimod interferes with the metastatic process, presumably by inhibition of tumor establishment. Therefore, tasquinimod is an interesting treatment option for patients with prostate cancer prone to metastasis.

Safety of Abiraterone Acetate in Castration-resistant Prostate Cancer Patients With Concomitant Cardiovascular Risk Factors

“…[15][16][17] Other agents such as radium-223, enzalutamide, cabozantinib, orteronel, and tasquinimod are being investigated for inclusion in the therapeutic armamentarium for mCRPC. 18,19 Therefore, physicians need to optimize the use of anticancer agents on the basis of age, comorbidities, and life expectancy of their patients. In this context, the availability of a well-tolerated agent could represent an opportunity to maintain a good quality of life in patients during and after therapy.…”

The HIF1A functional genetic polymorphism at locus +1772 associates with progression to metastatic prostate cancer and refractoriness to hormonal castration

“…These patients could also be enrolled in clinical trials with drugs that target HIF1a function (e.g. tasquinimod and other agents that target HIF1a or its downstream products) [34][35][36][37]. Present findings should be further extended and replicated by future studies focusing on genetic polymorphisms as predictors of treatment response to allow tailored therapy in PCa patients.…”

Long-term Survival and Biomarker Correlates of Tasquinimod Efficacy in a Multicenter Randomized Study of Men with Minimally Symptomatic Metastatic Castration-Resistant Prostate Cancer

“…For example, although immune therapies have reported improvements in OS without a noticeable impact on PFS (2, 24), antiangiogenic therapies have reported significantly improved PFS without an increase in OS (25). In addition to its antimetastatic properties (17, 26), tasquinimod has both immunomodulatory (10) and VEGF-independent antiangiogenic properties (7); therefore, the relationship of PFS improvement with OS for tasquinimod at present is not clear and requires adequately powered studies to address.…”

“…Another possibility is that bone-metastatic disease may have a different biology that leads to a greater benefit with tasquinimod. Preclinical models of PC treated with tasquinimod have demonstrated favorable effects in reducing or delaying both bone and visceral metastatic disease (26). As S100A9 is expressed in bone, and deficient mice have defective osteoclast activity, one hypothesis is that modulating the myeloid components surrounding a bone metastasis with tasquinimod may reduce pathologic bone resorption and skeletal events over time (30, 31).…”