New Data Demonstrating Long-term Benefits of FIRMAGON® (degarelix) for Advanced Hormone-dependant Prostate Cancer Published in The Journal of Urology

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Ferring

31 Aug, 2011, 06:00 GMT

SAINT-PREX, Switzerland, August 31, 2011 /PRNewswire/ --

- Rapid and sustained testosterone suppression and improved PSA control may delay time to second-line therapy

New data, published in the September issue of The Journal of Urology, showed that long-term use of FIRMAGON® (degarelix) a gonadotropin-releasing hormone therapy (GnRH) approved for the treatment of advanced prostate cancer in both the EU and US, continued to be effective and well tolerated beyond three years.[1]  The new study (CS21A) extends the conclusions of the pivotal Phase III study (CS21) in which the risk of prostate-specific antigen (PSA) failure or death was significantly lower in patients on FIRMAGON® compared to leuprolide (an LHRH agonist) up to one year.[1] The extension study has now shown that for patients who remained on FIRMAGON®, PSA suppression and the effects on PSA progression free survival (PFS) remained consistent over the long term (42 months).[1]

In addition, the study looked at patients who crossed over from leuprolide to FIRMAGON®after one year.  At a median follow up of 27.5 months the data showed that the risk of PSA PFS had decreased (p=0.003).[1]  

Longer PSA PFS is desirable as it is indicative of time to castration-resistant prostate cancer (CRPC) and may delay initiation of second-line therapy, which includes chemotherapy.[2] Time to castration resistance is also an important predictor of survival.[3]  These findings support using FIRMAGON® as first-line androgen deprivation therapy.[1]

CS21A was designed to collect extended safety and tolerability data on FIRMAGON®. Following the close of the Phase III trial, all patients were offered the option to receive FIRMAGON® as part of the extension study. All patients who had received FIRMAGON® continued with their treatment and those who had previously been treated with leuprorelin were re-randomised to receive FIRMAGON®.

"Being able to delay castration resistance for as long as possible is an important outcome for any first-line therapy," said E. David Crawford, MD, Head, Section of Urologic Oncology and Professor of Urologic and Radiation Oncology, University of Colorado Denver, US. "The data from the Phase III extension study demonstrate that FIRMAGON® provided prostate cancer patients with fast and effective testosterone and PSA control over the long term, which may in turn delay castration resistance."  

Prostate cancer is the second leading cause of cancer death amongst men in the Western world.[4] Up to 40% of men diagnosed with prostate cancer will eventually develop advanced disease, and although most respond to initial medical or surgical castration, progression to CRPC is inevitable.[5] The average survival for patients with CRPC is two to three years.[5]

FIRMAGON® works by immediately inhibiting the GnRH receptors in the pituitary gland and suppressing the luteinising hormone, which decreases production of testosterone by the testicles with no initial surge. Prostate cancer is dependent on testosterone for its growth, so the goal of therapy is to rapidly reduce testosterone levels to slow the growth of cancer cells. Avoiding flare in testosterone prevents initial worsening of clinical status, allows for faster relief of symptoms such as bone pain, ureteral obstruction, and spinal cord compression and removes the need for adjuvant treatment with anti-androgens.[6,7,8]

Further information

FIRMAGON® (degarelix) is a new medication indicated for the treatment of advanced hormone-dependent prostate cancer.

For additional information on Firmagon® or Ferring Pharmaceuticals please contact Ferring International Center S.A. Ch. de la Vergognausaz 50, 1162 Saint-Prex, Switzerland Tel:  +41 58 301 00 00 / Fax: +41 58 301 00 10, or visit http://www.ferring.com/en/global/Contact+Us.htm

References

1. Crawford, ED  et al. The Journal of Urology September 2011;186(3):889-897

2. Mahon KL, et al. Endocr Relat Cancer 2011;18:R103-R123

3. Bournakis E, et al. Icancer Res 2011: Apr;31(4):1475-82 http://www.ncbi.nlm.nih.gov/pubmed/21508406   

4. American Cancer Society. Available at: http://www.cancer.org/docroot/cri/content/cri_2_4_1x_what_are_the_key_statistics_for_prostate_cancer_36.asp [Accessed 25 May 2010]

5. Beltran, H et al. European Urology 60(2011) 279-290 http://www.europeanurology.com/article/S0302-2838(11)00477-5/pdf/New+Therapies+for+Castration-Resistant+Prostate+Cancer%3A+Efficacy+and+Safety

6. Van Poppel, H et al. Urology: June 2009; Volume 71, Issue 6:1001-1006 http://www.goldjournal.net/article/S0090-4295(07)02662-3/abstract

7. Persson B-E, et al. Neuroendocrinology 2009;90:235-244

8. Boccon-Gibod L, et al. Therap Adv Urol June 2011