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A Study of Anlotinib Hydrochloride Capsule Combined With Chemotherapy as First-line Treatment in Subjects With RAS/BRAF Wild Metastatic Colorectal Cancer

ABSTRACT: This is an open label, randomized, phase Ⅲ study to treat subjects with RAS/BRAF wild-type, unresectable metastatic colorectal cancer. The patients will be randomized into two arms consist of Anlotinib (3 weeks/cycle) + CapeOx and Bevacizumab (3 week/cycle) + CapeOx at a ratio of 1:1. This study is conducted to assess the efficacy and safety of Anlotinib and Chemotherapy as first-line treatment in subjects with RAS/BRAF wild-type Metastatic Colorectal Cancer.

DISEASE(S): Metastatic Colorectal Cancer,Colorectal Neoplasms

PROVIDER: 2375058 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Anlotinib Hydrochloride Capsules Combined With CAPEOX in RAS and BRAF Wild-type mCRC Patients

Project description:This is an Open, Single Arm, Exploratory and Phase II Clinical Trial of Anlotinib Hydrochloride Capsules Combined With CAPEOX in RAS and BRAF wild-type patients with Metastatic Colorectal Carcinoma(CRC) as 1st Therapy. After 6 cycles of combined therapy, patients will receive capecitabine and anlotinib as maintenance therapy until tumor progression.In order to observe and evaluate the efficacy and safety of Anlotinib Hydrochloride Capsules combined with CAPEOX in treatment of patients with mCRC. The patients who are pathologically confirmed as RAS and BRAF wild-type mCRC will be enrolled. Condition or disease Invention/treatment Phase Colorectal Cancer Drug: Anlotinib Hydrochloride Drug: Capecitabine Drug: Oxaliplatin Phase 2

| 2315608 | ecrin-mdr-crc

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Further to our previous study (E-MTAB-5997), here we performed transcriptome profiling on Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975, and would like to understand the effects of Anlotinib on Anlotinib-resistant NCI-H1975 cell, compare the different transcriptome profiling on NCI-H1975 cells and Anlotinib-resistant NCI-H1975 cells, sought to find the biomarker for explaining Anlotinib resistance.

2019-07-01 | E-MTAB-7068 | biostudies-arrayexpress

Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

Project description:Anlotinib, a multitarget agent a multi-target agent that inhibits tumor proliferation and angiogenesis, has been demonstrated to be effective for non-small cell lung cancer (NSCLC) at third-line or over third-line. However, the underlying mechanisms of anlotinib acquired-resistance is still unclear. Here we performed chromatin accessibility profiling on anlotinib-resistant NCI-H1975 and wild-type NCI-H1975. By integrating with transcriptome analysis, we found that anlotinib resistance was due to increased angiogenic capacity, and revealed that TFAP2A was involved in anlotinib resistance. Next, TFAP2A was knock-down in anlotinib-resistant cells and RNAseq was performed to see down-regulated genes with TFAP2A KD.

2020-11-09 | GSE142031 | GEO

Next-generation sequencing quantitative analysis of the transcriptome of intrahepatic cholangiocarcinoma cell line treated with or without anlotinib.

Project description:To examine the potential mechanism of anlotinib to inhibit intrahepatic cholangiocarcinoma, we used RNA-seq to analyze the effect of anlotinib treatment on the transcriptome changes of intrahepatic cholangiocarcinoma cell lines HCCC9810 and RBE. HCCC9810 and RBE cells were treated with DMSO or anlotinib at 5 μM for 24 hours, and then subjected to total RNA isolation and deep sequencing. We used Venn diagrams of RNA-seq results of HCCC9810 and RBE cells treated with anlotinib to indicate genes that were up- or down-regulated (adjusted P value <0.05, fold = 2.0). There are 420 genes in both groups (Figure 4A, 273 genes up-regulated and 147 genes down-regulated). In summary, the above sequencing results were analyzed by bioinformatics, and it was concluded that by inactivating the VEGF / PI3K / AKT signaling pathway and through cell cycle arrest, anlotinib treatment inhibited the proliferation and invasion of tumor cells and promoted Apoptosis.

2021-05-01 | GSE149901 | GEO

A Clinical Study to Compare the Efficacy and Safety of AK105 Plus Anlotinib and Capecitabine/Oxaliplatin (CapeOx) , Anlotinib Plus CapeOx, Bevacizumab Plus CapeOx

Project description:A clinical study to compare the efficacy and safety of AK105 plus anlotinib and Capecitabine/Oxaliplatin (CapeOx) , anlotinib plus CapeOx, bevacizumab plus CapeOx. A total of 120 cases will be enrolled to the group.

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Gene expression after human SW982 cells treated with anlotinib by a microarray profiling (Affymetrix)

Project description:Anlotinib could significantly suppresses synovial sarcoma proliferation in PDTX model and cell lines. To identify potential anlotinib targets in synovial sarcoma, we performed a microarray profiling (Affymetrix) in human SW982 cells treated with anlotinib.

2019-01-01 | GSE109468 | GEO

Gene expression after human PANC-1 cells treated with anlotinib by a microarray profiling (Affymetrix)

Project description:Anlotinib exerted cytotoxity on pancreatic cancer cells. To identify potential anlotinib targets in pancreatic cancer, we performed a microarray profiling (Affymetrix) in human PANC-1 cells treated with anlotinib.

2020-12-21 | GSE163574 | GEO

Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

Project description:Transcriptome profiling of Anlotinib-resistant NCI-H1975 and Anlotinib-treated Anlotinib-resistant NCI-H1975

| PRJEB27916 | ENA

Role of Anlotinib-induced CCL2 decrease in anti-angiogensis and response prediction for Non-Small Cell Lung Cancer therapy

Project description:Purpose: Our previous clinical trials have been demonstrated that Anlotinib can inhibit tumor growth upon refractory advanced non-small cell lung cancer (NSCLC) patients with the possibility mechanism of anti-angiogenesis. The present study sought to reveal the underlying molecular mechanism of Anlotinib-induced anti-angiogenesis in advanced NSCLC. Experimental Design: Computed tomography (CT) was used to evaluate the treatment effect of Anlotinib upon refractory advanced NSCLC patients. Transcriptome profiling was performed to identify the key gene expression alteration in NCI-H1975 cells before and after Anlotinib treatment. NCI-H1975 derived xenograft model was applied to investigate treatment effect and verify anti-angiogenesis mechanism of Anlotinib. Results: Anlotinib induces tumor cytotoxicity on refractory advanced NSCLC patients, NCI-H1975 derived xenograft models and lung adenocarcinoma cell lines. Transcriptome profiling revealed CCL2 blockade could be responsible for Anlotinib-induced anti-angiogenesis. NCI-H1975 derived xenograft model demonstrated Anlotinib-induced CCL2 blockade play an important role in anti-angiogenesis. Conclusions: This study not only offered the first evidence that Anlotinib inhibits angiogenesis via blocking CCL2 expression, but also provided a novel theoretical basis for the application of Anlotinib in advanced NSCLC patients.

2018-11-30 | E-MTAB-5997 | biostudies-arrayexpress

Enhancing Tumor Targeting of Antitumor Drugs through Anlotinib-Mediated Modulation of Extracellular Matrix and RhoA/ROCK Signaling Pathway

Project description:In this study, our research focused on investigating the impact of Anlotinib in enhancing the tumor targeting of antitumor drugs in vivo. Through RNA-sequencing and Label-free quantitative proteomics analysis, we discovered that Anlotinib effectively regulated the expression of extracellular matrix (ECM) genes and proteins, leading to a significant reduction in ECM stiffness. Our bioinformatic analysis indicated a potential positive relationship between the ECM pathways and gefitinib resistance, poor PD-1 treatment outcomes, as well as unfavorable prognosis in lung cancer patients following chemotherapy. To evaluate the efficacy of Anlotinib, we administered it in combination with anti-PD-1/PD-L1 agents, chemotherapeutic drugs, and gefitinib, and visualized their distribution using fluorescent labeling in various tumor types. Notably, our results demonstrated that Anlotinib substantially improved the drug targeting process by prolonging the retention time of antitumor drugs at the tumor site. Moreover, the combination therapy induced a notable loosening of the tumor tissue structure compared to the control group. This reduction in stiffness was further associated with decreased interstitial fluid pressures and tumor solid pressure. Additionally, we observed that Anlotinib effectively suppressed the RhoA/ROCK signaling pathway, inhibiting the formation of stress fibers. These findings strongly suggest that Anlotinib enhances the distribution and retention of antitumor drugs in tumors by modulating ECM expression and physical properties through the RhoA/ROCK signaling pathway. These valuable insights contribute to the development of combination therapies aimed at improving tumor targeting in cancer treatment.

2024-07-31 | GSE237818 | GEO

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