There has been a recent thread on modified citrus pectin [MCP], & I have an old post thart reviewed the literature. For most of us MCP means PectaSol.
The study was on 35 "non-metastatic biochemically relapsed prostate cancer ... patients (pts)". Treatment (tx): "4.8 grams X 3/day"
"62% (n = 21) had a stabilization/decrease of PSA, and negative scans, at 6 mos, and entered the second 12 mos tx phase."
"A stabilization or improvement (increase) of PSA doubling time was noted in 79% (n = 27) of pts. Disease progression at 6 mos was noted in 38% (n = 13: PSA only 29%, n = 10; PSA and scans 9%, n = 3)."
"The present study suggests a potential benefit of P-MCP ..."
14 Poster Session (Board #A20), Thu, 11:30 AM-1:00 PM and
5:15 PM-6:15 PM
Effect of pectasol-c modified citrus pectin (P-MCP) treatment (tx) on PSA dynamics in non- metastatic biochemically relapsed prostate cancer (BRPC) patients (pts): Results of a prospective phase II study.
Daniel Keizman, Moshe A. Frenkel, Avivit Peer, Eli Rosenbaum, David Margel, David Leonid Sarid, Victoria Neiman, Maya Gottfried, Natalie Maimon, Ilan Leibovitch, Hadas Dresler, Isaac Eliaz; Meir Medical Center, Kfar-Saba, Israel; Rambam Health Care Campus, Haifa, Israel; Davidoff Cancer Center, Petah Tikva, Israel; Rabin Medical Center, Petah Tikva, Israel; Ichilov Medical Center, Tel Aviv, Israel; Davidoff Cancer Center, Rabin Medical Center, Petah Tikva, Israel; Lung Cancer Unit, Meir Medical Center, Kfar-Saba, Israel; Meir Medical Center, Sackler School of Medicine, Tel Aviv University, Kfar-Saba, Israel; Amitabha Medical Clinic and Healing Center, Santa Rosa, CA
Background: 30% of pts with localized PC will have a biochemical relapse post local tx. The optimal tx of these pts remains elusive. While androgen deprivation therapy is effective in reducing PSA level, its long-term benefit on survival remain undefined, and it is associated with significant cumulative toxicities.Thus, evaluation of new non-toxic compounds in this pt population is warranted. P-MCP is a competitive inhibitor of galectin-3, a carbohydrate-binding protein, which is known to be involved in cancer pathogenesis. Pre-clinical and clinical data suggest that P-MCP is active in PC. We aimed to evaluate the safety and PSA dynamics of tx with P-MCP in pts with BRPC.
Methods: Pts with non-castrate non-metastatic BRPC were enrolled in a prospective phase 2 study of tx with oral P-MCP, at 4.8 grams X 3/day for 6 months (mos). Pts that did not progress clinically, biochemically (PSA), and radiologically, at 6 mos, were treated for subsequent 12 mos. Sample size provided 85% power to assess a decrease in PSA progression rate from 80% (natural history) to 40% (P-MCP tx) at 6 mos.
Results: The study was initiated in June 2013. 35 pts were enrolled. Median age was 74 years. Treatment of the primary tumor consisted of surgery in 11% (n = 4), radiation in 69% (n = 24), and both in 20% (n = 7). No pt had tx related grade 3/4 toxicity. One patient withdrew his consent after 1 mos. Of the 34 pts analyzed, 18% (n = 6) had grade 1 toxicity. 62% (n = 21) had a stabilization/decrease of PSA, and negative scans, at 6 mos, and entered the second 12 mos tx phase. A stabilization or improvement (increase) of PSA doubling time was noted in 79% (n = 27) of pts. Disease progression at 6 mos was noted in 38% (n = 13: PSA only 29%, n = 10; PSA and scans 9%, n = 3).
Conclusions: The present study suggests a potential benefit of P-MCP tx on progression of BRPC. P-MCP tx is safe. Clinical trial information: NCT01681823.