About Non Small Cell Lung Carcinoma (NSCLC)
Non-small-cell lung carcinoma (NSCLC) is any type of epithelial lung cancer other than small-cell lung carcinoma (SCLC). NSCLC accounts for about 85% of all lung cancers. As a class, NSCLCs are relatively insensitive to chemotherapy, compared to small-cell carcinoma. When possible, they are primarily treated by surgical resection with curative intent, although chemotherapy has been used increasingly both preoperatively (neoadjuvant chemotherapy) and postoperatively (adjuvant chemotherapy).
4 kinds of targeted drugs for the treatment of About ROS1-positive non-small cell lung cancer can be made in Laos
Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do. Monoclonal antibodies, tyrosine kinase inhibitors, and mammalian target of rapamycin (mTOR) inhibitors are three types of targeted therapy being used to treat advanced, metastatic, or recurrent non-small cell lung cancer.
ROS1 is a receptor tyrosine kinase (encoded by the c-Ros oncogene) that shares structural similarity with the anaplastic lymphoma kinase (ALK) protein.
Crizotinib is indicated for the treatment of metastatic non-small cell lung cancer (NSCLC) or relapsed or refractory, systemic anaplastic large cell lymphoma (ALCL) that is ALK-positive. It is also indicated for the treatment of unresectable, recurrent, or refractory inflammatory anaplastic lymphoma kinase (ALK)-positive myofibroblastic tumors (IMT).
|Drug Profile||Crizotinib is an inhibitor of receptor tyrosine kinases including ALK, Hepatocyte Growth Factor Receptor (HGFR, c-Met), ROS1 (c-ros), and Recepteur d’Origine Nantais (RON). Translocations can affect the ALK gene resulting in the expression of oncogenic fusion proteins. The formation of ALK fusion proteins results in activation and dysregulation of the gene’s expression and signaling which can contribute to increased cell proliferation and survival in tumors expressing these proteins. Crizotinib demonstrated concentration-dependent inhibition of ALK, ROS1, and c-Met phosphorylation in cell-based assays using tumor cell lines and demonstrated antitumor activity in mice bearing tumor xenografts that expressed echinoderm microtubule-associated protein-like 4 (EML4)- or nucleophosmin (NPM)-ALK fusion proteins or c-Met.|
|Alternative Names||PF-002341066; PF-02341066; PF-1066; PF-2341066; Xalkori|
|Developer||Astellas Pharma; Children’s Oncology Group; Dana-Farber Cancer Institute; National Cancer Institute (USA); OxOnc Development; Pfizer; University of Colorado at Denver; University of Milan Bicocca|
|Class||Antineoplastics; Chlorobenzenes; Fluorobenzenes; Piperidines; Pyrazoles; Pyridines; Small molecules|
|Mechanism of Action||Anaplastic lymphoma kinase inhibitors; Proto oncogene protein c met inhibitors; ROS1 protein inhibitors|
|Orphan Drug Status||Yes – Neuroblastoma; Non-small cell lung cancer; Non-Hodgkin’s lymphoma|
|Patent Information||There are five patents protecting this compound. Crizotinib has one hundred and fifty patent family members in forty-seven countries.|
A drug used to treat adults with non-small cell lung cancer that has spread and is ALK positive. It is also being studied in the treatment of other types of cancer. Ceritinib blocks certain proteins made by the ALK gene. Blocking these proteins may stop the growth and spread of cancer cells. Ceritinib is a type of tyrosine kinase inhibitor. Also called Zykadia.
|Drug Profile||Ceritinib is a kinase inhibitor. Targets of ceritinib inhibition identified in either biochemical or cellular assays at clinically relevant concentrations include ALK, insulin-like growth factor 1 receptor (IGF-1R), insulin receptor (InsR), and ROS1. Among these, ceritinib is most active against ALK. Ceritinib inhibited autophosphorylation of ALK, ALK-mediated phosphorylation of the downstream signaling protein STAT3, and proliferation of ALK-dependent cancer cells in in vitro and in vivo assays.|
|Alternative Names||Jikadia; LDK-378; NVP-LDK 378; NVP-LDK378-NX; Zykadia|
|Developer||H. Lee Moffitt Cancer Center and Research Institute; Novartis; University of Texas Southwestern Medical Center|
|Class||Antineoplastics; Diamines; Piperidines; Pyrimidines; Small molecules; Sulfones|
|Mechanism of Action||Anaplastic lymphoma kinase inhibitors|
|Orphan Drug Status||Yes – Non-small cell lung cancer|
|Patent Information||There are eleven patents protecting this compound. Ceritinib has three hundred and eighty-five patent family members in fifty-five countries.|
A drug used to treat adults with non-small cell lung cancer that has spread to other parts of the body and is ALK positive. It is also being studied in the treatment of other types of cancer. Lorlatinib blocks certain proteins made by the ALK gene. Blocking these proteins may stop the growth and spread of cancer cells.
|Drug Profile||Lorlatinib is a kinase inhibitor with in vitro activity against ALK and ROS1 as well as TYK1, FER, FPS, TRKA, TRKB, TRKC, FAK, FAK2, and ACK. Lorlatinib demonstrated in vitro activity against multiple mutant forms of the ALK enzyme, including some mutations detected in tumors at the time of disease progression on crizotinib and other ALK inhibitors.|
|Alternative Names||[14C]Lorlatinib; LORBRENA; LORVIQUA; Lorviqua; PF-06463922; PF-6463922|
|Developer||CStone Pharmaceuticals; New Approaches to Neuroblastoma Therapy Consortium; Pfizer; The EVAN Foundation; University of Southern California|
|Class||Antineoplastics; Aza compounds; Benzoxazines; Nitriles; Pyrazoles; Pyridines; Small molecules|
|Mechanism of Action||Anaplastic lymphoma kinase inhibitors; ROS1 protein inhibitors|
|Orphan Drug Status||Yes – Non-small cell lung cancer|
|Patent Information||There are four patents protecting this compound. Lorlatinib has ninety-five patent family members in forty-seven countries.|
A drug used in adults to treat non-small cell lung cancer that has spread and is ROS1 positive and in adults and children aged 12 years and older to treat solid tumors that have certain changes in the NTRK gene. It is also being studied in the treatment of other types of cancer. Entrectinib blocks certain proteins involved in cell signaling and cell growth. Blocking these proteins may help keep cancer cells from growing and may kill them.
|Drug Profile||Entrectinib is an inhibitor of the tropomyosin receptor tyrosine kinases (TRK) TRKA, TRKB, and TRKC (encoded by the neurotrophic tyrosine receptor kinase [NTRK] genes NTRK1, NTRK2, and NTRK3, respectively), proto-oncogene tyrosine-protein kinase ROS1 (ROS1), and anaplastic lymphoma kinase (ALK).|
|Alternative Names||Entrectinib – Ignyta; NMS-E628; RG 6268; Rozlytrek; RXDX-101; TrkA/TrkB/TrkC/ROS1/ALK inhibitor – Roche|
|Originator||Nerviano Medical Sciences|
|Developer||Alliance for Clinical Trials in Oncology; Chugai Biopharmaceuticals; Genentech; National Cancer Institute (USA); Roche; University of California at San Francisco|
|Class||Antineoplastics; Benzamides; Fluorinated hydrocarbons; Indazoles; Piperazines; Pyrans; Small molecules; Tumour-agnostic therapies|
|Mechanism of Action||Anaplastic lymphoma kinase inhibitors; ROS1 protein inhibitors; TrkA receptor antagonists; TrkB receptor antagonists; TrkC receptor antagonists|
|Orphan Drug Status||Yes – Neuroblastoma; Colorectal cancer; Solid tumours; Non-small cell lung cancer|
|Patent Information||There are fourteen patents protecting this compound. Entrectinib has one hundred and fifteen patent family members in twenty-nine countries.|
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The WTO’s Council for Trade-Related Aspects of Intellectual Property Rights (TRIPS) ：Under this license, the Lao pharmaceutical industry, as well as the pharmaceutical industry in similar countries（Bangladesh, Nepal, etc.）, will be able to manufacture many drugs without patent authorization.Reference：
《WTO members agree to extend drug patent exemption for poorest members》https://www.wto.org/english/news_e/news15_e/trip_06nov15_e.htm
《Product Patent Protection, the TRIPS LDC Exemption and the Bangladesh Pharmaceutical Industry》https://www.twn.my/title2/IPR/pdf/ipr17.pdf