Approval Probability
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Adjusted LOA
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Standard taxane therapy · 1 trial · 1 indication
Progression was defined as an increase by at least 20 percent (%) from the smallest value in the Sum of Longest Diameter (SLD) of lesions. Biomarkers investigated: p95 human epidermal growth factor receptor 2 (p95HER2) positive (+ve) and negative (-ve) , insulin growth factor-1 receptor (IGF1R) less than (\<) median and greater than or equal to (≥) median membrane H score, c-MET \<median and ≥median membrane H score, phosphatase and tensin homolog gene (PTEN) \<median and ≥median cytoplasm H score, HER2 \<median and ≥median membrane H score, phosphatidylinositol-3-kinase (PI3K) catalytic subunit wild type (WT) and mutation (M), and FC gamma receptors IIIa homozygous Phenyl alanine (FF), heterozygous Phenyl alanine/Valine (VF) and homozygous Valine (VV), receptor IIa Phenotypes homozygous Histidine (HH), heterozygous Histidine/Arginine (HR) and homozygous Arginine (RR) IIb phenotypes homozygous Isoleucien (II),heterozygous Isoleucine/Threonine (IT) and homozygous Threonine (TT) .
PFS was calculated from first study medication in Part II to date of progression or death.The relationship between PFS and the following biomarker variables was investigated in each of study Part 1 and 2: p95HER2 +ve and -ve population, IGF1R \<median and ≥ median membrane H score, c-MET \<median and ≥median membrane H score, PTEN \<median and ≥median cytoplasm H score, HER2 \<median and ≥median membrane H score, PI3K catalytic subunit WT and M, and FC gamma receptors IIIa, IIa and IIb Phenotypes FF, VF and VV, HH, HR and RR, and II, IT and TT.
Progression was defined as an increase by at least 20% from the smallest value in the SLD of lesions.TTP was determined as the time in months from the date of screening until first progression.The relationship between PFS and the following biomarker variables was investigated in each of study Part 1 and 2: p95 HER2 +ve and -ve population, IGF1R \<median and ≥median, c-MET \<median and ≥median, PTEN \<median and ≥median, HER2 \<median and ≥median, PI3K catalytic subunit WT and M, and FC gamma receptors IIIa, IIa and IIb Phenotypes FF, VF and VV, HH, HR and RR, and II, IT and TT . The correlation between the biomarker variables and TTP were investigated using a univariate Cox regression model and time-to-event methods (Kaplan-Meier).
TTP was calculated from first study medication in Part II to date of progression. The relationship between TTP and the following biomarker variables was investigated in each of study Part 1 and 2: p95 HER2 +ve and -ve population, IGF1R \<median and ≥median, c-MET \<median and ≥median, PTEN \<median and ≥median, HER2 \<median and ≥median, PI3K catalytic subunit WT and M, and FC gamma receptors IIIa, IIa and IIb Phenotypes FF, VF and VV, HH, HR and RR, and II, IT and TT .
BOR was defined according to the Response Evaluation Criteria In Solid Tumors (RECIST). CR: disappearance of all target lesions and all pathological lymph nodes below 10 mm. PR: At least a 30% decrease in the sum of diameters of target lesions. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. PD: At least a 20% increase in the sum of diameters of target lesions, and the sum must also demonstrate an absolute increase of at least 5 mm or persistence of non-target lesions. The relationship between best response and the following biomarkers was investigated: p95 HER2 (+ve/-ve), IGF1R, c-MET, PTEN, HER2 (median/≥median), PI3K catalytic subunit (WT/M), and FC gamma receptors IIIa, IIa and IIb (phenotypes FF, VF, VV, HH, HR, RR and II, IT and TT respectively). The correlation between the biomarker variables and percentage of participants with best response were investigated using a univariate regression analysis.
Best Overall response was defined according to RECIST. CR: disappearance of all target lesions and all pathological lymph nodes below 10 mm.PR: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters. SD: Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD. PD: At least a 20% increase in the sum of diameters of target lesions, and the sum must also demonstrate an absolute increase of at least 5 mm or persistence of non-target lesions. The relationship between best response and the following biomarkers was investigated: p95 HER2 (+ve/-ve), IGF1R, c-MET, PTEN, HER2 (\<median/≥median) , PI3K catalytic subunit (WT/M), and FC gamma receptors IIIa, IIa and IIb (phenotypes FF, VF, VV, HH, HR, RR and II, IT and TT respectively). The correlation between the biomarker variables and percentage of participants with best response were investigated using a univariate regression analysis.
| Arm | Type | Description |
|---|---|---|
| 1 | EXPERIMENTAL | - |
| Name | Type | Description |
|---|---|---|
| Standard taxane therapy | DRUG | As prescribed |
| capecitabine [Xeloda] | DRUG | 1000mg/m2 po bid on days 1-14 of each 3-week cycle (only in patients who have progressed) |
| trastuzumab [Herceptin] | DRUG | 8mg/kg iv loading dose on day 1 of first 3-week cycle, and 6mg/kg iv on day 1 of each subsequent cycle |
Inclusion Criteria: * female patients, \>=18 years of age; * HER2-positive breast cancer; * al least one metastatic site amenable for core biopsy; * left ventricular ejection fraction \>50%. Exclusion Criteria: * prior adjuvant/neoadjuvant Herceptin within past 6 months; * prior adjuvant taxane t...
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Standard taxane therapy is a small molecule oncology treatment studied for use in breast cancer. It was evaluated in a Phase 2 clinical trial for patients with HER2-positive metastatic breast cancer. The trial has been completed, and the therapy remains investigational for this indication.
Standard taxane therapy is developed by Roche Holding AG, which trades under the ticker RHHBY. The company conducted a Phase 2 clinical trial of the therapy in patients with HER2-positive metastatic breast cancer. The trial has been completed.
Standard taxane therapy is in Phase 2 clinical development for breast cancer. It has completed one Phase 2 trial, which was an uncontrolled study of 33 female patients with HER2-positive metastatic breast cancer. The therapy is investigational and not yet approved.
Standard taxane therapy has been studied in one completed clinical trial, NCT00885755, titled 'A Study of Herceptin (Trastuzumab) and Biomarkers in Patients With HER2-Positive Metastatic Breast Cancer.' This Phase 2 trial enrolled 33 female patients aged 18 years and older across Australia, Spain, Sweden, and the United Kingdom.
Standard taxane therapy is not the same as Herceptin (trastuzumab). The completed clinical trial NCT00885755 studied Standard taxane therapy in combination with Herceptin and biomarkers in patients with HER2-positive metastatic breast cancer. Standard taxane therapy is a separate small molecule treatment.