A Phase II Study Evaluating the Efficacy and Safety of Combination of CPGJ602 and Chemotherapy as First Line Treatment in KRAS/NRAS/BRAF Wild-type, Metastatic Colorectal Cancer Patients

To assess the efficacy and safety of the combination of CPGJ602 and chemotherapy in subjects with KRAS/NRAS/BRAF wild-type, metastatic colorectal cancer.

Start Date07 Dec 2020

Sponsor / Collaborator

Sunshine Guojian Pharmaceutical (Shanghai) Co., Ltd.

CTR20201283 / Active, not recruitingPhase 2

评价CPGJ602联合mFOLFOX6 一线治疗KRAS/NRAS/BRAF野生型转移性结直肠癌有效性和安全性的Ⅱ期临床研究

[Translation] A phase II clinical study to evaluate the efficacy and safety of CPGJ602 combined with mFOLFOX6 as first-line treatment for KRAS/NRAS/BRAF wild-type metastatic colorectal cancer

初步评价 CPGJ602 两种给药方案与爱必妥®分别联合 mFOLFOX6 治疗KRAS/NRAS/BRAF 野生型转移性结直肠癌患者的有效性，安全性和耐受性，包括免疫原性。并评价CPGJ602 两种给药方案的群体药代动力学特征及暴露效应关系分析及考察循环肿瘤 DNA动态变化对于CPGJ602 和爱必妥®的疗效是否存在影响。

[Translation]

The aim is to preliminarily evaluate the efficacy, safety and tolerability, including immunogenicity, of two dosing regimens of CPGJ602 and Erbitux® in combination with mFOLFOX6 in the treatment of patients with KRAS/NRAS/BRAF wild-type metastatic colorectal cancer. The aim is to evaluate the population pharmacokinetic characteristics and exposure-effect relationship analysis of the two dosing regimens of CPGJ602 and investigate whether the dynamic changes of circulating tumor DNA affect the efficacy of CPGJ602 and Erbitux®.

Start Date07 Dec 2020

Sponsor / Collaborator

Sunshine Guojian Pharmaceutical (Shanghai) Co., Ltd.

CTR20190958 / CompletedPhase 1

重组抗EGFR人鼠嵌合单克隆抗体注射液与爱必妥？在健康男性志愿者中药代动力学特性、免疫原性和安全性比对研究

[Translation] Comparative study on the pharmacokinetic properties, immunogenicity and safety of recombinant anti-EGFR human-mouse chimeric monoclonal antibody injection and Erbitux in healthy male volunteers

主要目的：比较重组抗EGFR人鼠嵌合单克隆抗体注射液（以下简称CPGJ602）与爱必妥®在健康男性志愿者中的PK特征次要目的：比较CPGJ602与爱必妥®在健康男性志愿者中的安全性和免疫原性

[Translation]

Primary objective: To compare the PK characteristics of recombinant anti-EGFR human-mouse chimeric monoclonal antibody injection (hereinafter referred to as CPGJ602) and Erbitux® in healthy male volunteers Secondary objective: To compare the safety and immunogenicity of CPGJ602 and Erbitux® in healthy male volunteers

Start Date23 Jul 2019

Sponsor / Collaborator

Sunshine Guojian Pharmaceutical (Shanghai) Co., Ltd.

100 Clinical Results associated with P-gp x EGFRvIII

100 Translational Medicine associated with P-gp x EGFRvIII

0 Patents (Medical) associated with P-gp x EGFRvIII

Literatures (Medical) associated with P-gp x EGFRvIII

01 Oct 2014·Molecular Cancer TherapeuticsQ2 · MEDICINE

Temozolomide Induces the Production of Epidermal Growth Factor to Regulate MDR1 Expression in Glioblastoma Cells

Q2 · MEDICINE

Article

Author: Greco, Steven J. ; Munoz, Jessian L. ; Scotto, Kathleen W. ; Rodriguez-Cruz, Vivian ; Rameshwar, Pranela ; Nagula, Vipul

AbstractGlioblastoma multiforme (GBM) commonly resists the frontline chemotherapy treatment temozolomide. The multidrug resistance gene (MDR1) and its protein, P-glycoprotein (P-gp), are associated with chemoresistance. This study investigated the mechanisms underlying MDR1-mediated resistance by GBM to temozolomide. P-gp trafficking was studied by flow cytometry and Western blot analysis. MDR1 expression was analyzed by real-time PCR and reporter gene assays. AP-1 interaction with MDR1 was studied by chromatin immunoprecipitation assay. EGF production was analyzed by ELISA, EGFR signaling was determined by Western blot analysis, and in vivo response to erlotinib and/or temozolomide was studied in nude mice. During the early phase of temozolomide treatment, intracellular P-gp was trafficked to the cell membrane, followed by conformational change into active P-gp. At the later phase, gene transcription of MDR1 was induced by temozolomide-mediated production of EGF. EGF activated ERK1/2-JNK-AP-1 cofactors (c-jun and c-fos). An inhibitor of EGFR kinase (erlotinib) given to nude mice with GBM prevented temozolomide-induced resistance. The results identified an essential role for activated EGFR in the resistance of GBM to temozolomide. Temozolomide resistance occurred through a biphasic response; first, by a conformational change in P-gp into the active form and, second, by releasing EGF, which caused autocrine stimulation of GBM cells to induce MDR1. Pharmacologic inhibition of EGFR kinase blunted the ability of GBM cells to resist temozolomide. These findings may explain reports on the common occurrence of mutant EGFR (EGFRvIII) and EGFR expansion in the resistance of GBM cells. Mol Cancer Ther; 13(10); 2399–411. ©2014 AACR.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis