Trastuzumab is a humanizedIgG1monoclonal antibody for patients with invasive breast cancers that overexpress HER2. Trastuzumab has the potential for HER2 Positive Metastatic BreastCancerand HER2 Positive GastricCancerresearch.

Treatment of HER2-overexpressing breast cancer cell lines with Trastuzumab results in induction of p27KIP1 and the Rb-related protein, p130, which in turn significantly reduces the number of cells undergoing S-phase. A number of other phenotypic changes are observedin vitroas a consequence of Trastuzumab binding to HER2-overexpressing cells. Interaction of Trastuzumab with the human immune system via its human immunoglobulin G1 Fc domain may potentiate its antitumor activities.in vitrostudies demonstrate that Trastuzumab is very effective in mediating antibody-dependent cell-mediated cytotoxicity against HER2-overexpressing tumor targets^[1]. Trastuzumab consists of two antigen-specific sites that bind to the juxtamembrane portion of the extracellular domain of the HER2 receptor and that prevent the activation of its intracellular tyrosine kinase. Trastuzumab recruits immune effector cells that are responsible for antibody-dependent cytotoxicity^[2]. The presence of Trastuzumab IgG significantly increases killing of all breast cancer cell lines. The ADCC activity of PBMCs evoked by Trastuzumab is equally strong against Trastuzumab-sensitive (SKBR-3) or Trastuzumab-resistant (JIMT-1) breast cancer cells, with dose-dependent cell death reaching 50–60% killing at an effector/target ratio of 60:1^[3].

Trastuzumab treatment of mouse xenograft models results in marked suppression of tumor growth. When given in combination with standard cytotoxic chemotherapeutic agents, Trastuzumab treatment generally results in statistically superior antitumor efficacy compared with either agent given alone^[1]. Trastuzumab causes a significant growth inhibition of the outgrowth of macroscopic JIMT-1 xenograft tumors in both nude and SCID mice^[3].

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