r increases in NTX, CTX and DPD base with 10 mg atrasentan versus placebo metastatic CRPC 809 atrasentan 3-Methyladenine 10 mg QD compared to placebo, no reduction in risk of disease progression BAP average rose 13.2 ng / ml versus 33.9 ng / ml, P 0001 more time to PSA progression with atrasentan, the median time to progression BAP: 505 days vs 254 days, P 0.01 metastatic prostate cancer, 44-10 mg or 10 mg QD QD atrasentan atrasentan, more Zoledrons acid Q4W SD after 12 weeks in 3/22 in both arms, no significant differences in BAP changes in the mean serum NTX poor rose by 32.4% to 14.5%, decreased by 34, 4% to 6.9%, P 0.001 metastatic CRPC 31 atrasentan 10 mg QD plus docetaxel 60, 70 or 75 mg/m2 q21d PR in 2/13, best in SD 10/13 CONFIRMS BAP decreased median of 18 g / l to 12.2 g / l PSA response at 35% median NTX decreased from 12.
8 to 10.9 nM BCE nM BCE, P 0.
04 Zibotentan metastatic C Andarine RPC 16 10 200 mg QD Zibotentan intra-patient, no objective responses and considerable inter-individual variability of t in the BAP, PINP, CTX, NTX and metastatic CRPC dasatinib 47 mg twice t possible and 70 dasatinib 100 mg twice a lack of progress by RECIST and bone scintigraphy in 20/47 patients at week 12 and 9/47 patients at week 24 to 51% of patients had a 40% reduction in urinary NTX and 60% had a decrease in metastatic CRPC 48 BAP dasatinib 100 mg QD 12 patients had the contr the disease is 51% of patients had a 40% reduction in urinary NTX and 59% had a decrease in metastatic CRPC BAP dasatinib 46 mg QD 50 120 and docetaxel 65 mg/m2 or 75 q21d PR in 17/30 patients, 18 weeks in SD 5/30 49% of patients had had a 35% decrease in urine NTX and reducing the size e number of bones and a 73% reduction in L emissions BAP 6 weeks to 13/45 PSA response rate in 26 / Saracatinib 44 healthy volunteers in a single dose of 59 mg saracatinib 60 250, 10 July was followed days later Ter with t Adjusted doses from 10 to 14 days N / decrease from baseline in serum CTX, and uNTx TRACPb5 mg with 250 mg Extended CRPC 28 175 QD Saracatinib transient decrease in PSA in five patients undeclared denosumab solid tumors and bone metastases, with or without prior IV BP therapy Q4W BP 366, AW4 denosumab 30 mg, 120 mg AW4, 180 mg AW4, 60 mg or 180 mg Q12W reduce Q12W N / A uNTx median decrease of 75% or 80%, TRACP5b median of 73% of solid tumors and bone metastases, with BP before therapy Q4W IV BP 111, 180 mg of denosumab or 180 mg Q12W Q4W N / A uNTx median decrease of 78% reduction in serum CTX, PINP, TRACP5b, BAP, OC and prostate cancer and bone metastases, previous therapy with BP BP 50 Q4W IV, 180 mg of denosumab or 180 mg Q4W Q12W N / A 69% of patients had uNTx 50 nM, uNTx median decrease of 84% of BCE, the equivalent of bone collagen , BID, twice a day, CR, complete response, IV, by intravenous se N / A, not applicable, PR, partial response Q4W, every 4 weeks Q12W, every 12 weeks, q21d, t once every 21 days possible, once a day, RECIST, response criteria in solid tumors, SD, stable disease.
Bone markers in 690 prostate cancer and neoplasia Brown Sim flight. 12, No. 9, 2010 activation. Dasatinib is a potent inhibitor of SRC and the SRC family kinases and FMS, which also has activity against the receptor for platelet-derived growth factor, c-KIT and ABL. In vitro studies indicate that dasatinib activity t antiosteoclast more anti-tumor and anti-metastatic activity Th relative to the lines of prostate cancer cells. In two clinical studies in metastatic CRPC, treatment with dasatinib was entered Born in decreased bone turnover markers. In a study of the