lung permeability

By Targets:	EGFR (1) Furin (1) Interleukin Related (1) Phosphatase (1) Phosphodiesterase (PDE) (1) TRP Channel (1)
By Research Areas:	Cancer (2) Inflammation/Immunology (3) Neurological Disease (1)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-109061

Lazertinib 1 Publications Verification YH25448; GNS-1480	EGFR	Cancer
Lazertinib (YH25448) is a potent, highly mutant-selective, blood-brain barrier permeable, orally available and irreversible third-generation EGFR tyrosine kinase inhibitor, and can be used in the research of non-small cell lung cancer .

HY-16694

BAMB-4 ITPKA-IN-C14	Phosphatase	Cancer
BAMB-4 (ITPKA-IN-C14) is a specific and membrane-permeable ITPKA inhibitor. BAMB-4 has high stability and membrane permeability and against the inositol-1,4,5-trisphosphate (InsP3) kinase activity of inositol-1,4,5-trisphosphate-3-kinase A (ITPKA) with an IC₅₀ value of 20 μM. BAMB-4 can be used for the research of metastasis of lung cancer .

HY-147140

BOS-318	Furin	Inflammation/Immunology
BOS-318 is a potent, slowly dissociating, highly selective, and cell-permeable furin inhibitor with IC₅₀ value of 1.9 nM. BOS-318 protects ENaC from subsequent activation by neutrophil elastase. BOS-318 can be used for the rsearch for CF lung disease .

HY-131340

LASSBio-1632	Phosphodiesterase (PDE)	Inflammation/Immunology
LASSBio-1632 is a new anti-asthmatic lead candidate associated with selective inhibition of PDE4A and PDE4D isoenzymes and blockade of airway hyper-reactivity (AHR) and TNF-α production in the lung tissue. LASSBio-1632 (7j) displays high experimental BBB permeability across BBB through passive diffusion .

HY-149823

TRPV4 antagonist 4	TRP Channel	Neurological Disease
TRPV4 antagonist 4 is a potent TRPV4 antagonist with an IC₅₀ value of 22.65 nM. TRPV4 antagonist 4 inhibits TRPV4 current. TRPV4 antagonist 4 shows protective effects on acute lung injury .

HY-P1110

AF12198 1 Publications Verification	Interleukin Related	Inflammation/Immunology
AF12198 is a potent, selective and specific peptide antagonist for human type I interleukin-1 receptor (IL1-R1) (IC₅₀=8 nM) but not the human type II receptor (IC₅₀=6.7 µM) or the murine type I receptor (IC₅₀>200 µM). AF12198 inhibits IL-1-induced IL-8 production (IC₅₀=25 nM) and IL-1-induced intercellular adhesion molecule-1 (ICAM-1) expression (IC₅₀=9 nM) in vitro. AF12198 has anti-inflammatory activities and blocks responses to IL-1 in vivo .

Cat. No.	Product Name

HY-L075

Anti-Lung Cancer Compound Library	1835 compounds
Lung cancer is a major global health problem, as it is the leading cause of cancer-related deaths worldwide. Lung cancer is divided into two categories: small cell lung cancer and non-small cell lung cancer (NSCLC). Non-small cell lung cancer accounts for about 85 percent of lung cancers. As with all cancers, lung cancer may be treated with surgery, chemotherapy, radiation therapy, targeted therapy, immunotherapy or a combination thereof. Targeted therapy is one of the most exciting developments in lung cancer medicine, especially for NSCLC. Extensive genomic characterization of NSCLC has led to the identification of molecular subtypes of NSCLC that are oncogene addicted and exquisitely sensitive to targeted therapies. These include activating mutations in epidermal growth factor receptor (EGFR) and BRAF or echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusions and ROS1 receptor tyrosine kinase fusions. These are important targets for target therapy. MCE offers a unique collection of 1835 compounds with identified and potential anti-lung cancer activity. These compounds target lung cancer’s major targets and signaling pathways. MCE anti-lung cancer compound library is a useful tool for anti-lung cancer drugs screening and other related research.

Anti-Lung Cancer Compound Library

1835 compounds

Lung cancer is a major global health problem, as it is the leading cause of cancer-related deaths worldwide. Lung cancer is divided into two categories: small cell lung cancer and non-small cell lung cancer (NSCLC). Non-small cell lung cancer accounts for about 85 percent of lung cancers.

As with all cancers, lung cancer may be treated with surgery, chemotherapy, radiation therapy, targeted therapy, immunotherapy or a combination thereof. Targeted therapy is one of the most exciting developments in lung cancer medicine, especially for NSCLC. Extensive genomic characterization of NSCLC has led to the identification of molecular subtypes of NSCLC that are oncogene addicted and exquisitely sensitive to targeted therapies. These include activating mutations in epidermal growth factor receptor (EGFR) and BRAF or echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusions and ROS1 receptor tyrosine kinase fusions. These are important targets for target therapy.

MCE offers a unique collection of 1835 compounds with identified and potential anti-lung cancer activity. These compounds target lung cancer’s major targets and signaling pathways. MCE anti-lung cancer compound library is a useful tool for anti-lung cancer drugs screening and other related research.

Cat. No.	Product Name	Target	Research Area

HY-P1110

AF12198 1 Publications Verification	Interleukin Related	Inflammation/Immunology
AF12198 is a potent, selective and specific peptide antagonist for human type I interleukin-1 receptor (IL1-R1) (IC₅₀=8 nM) but not the human type II receptor (IC₅₀=6.7 µM) or the murine type I receptor (IC₅₀>200 µM). AF12198 inhibits IL-1-induced IL-8 production (IC₅₀=25 nM) and IL-1-induced intercellular adhesion molecule-1 (ICAM-1) expression (IC₅₀=9 nM) in vitro. AF12198 has anti-inflammatory activities and blocks responses to IL-1 in vivo .

MCE Japan Authorized Agent ナミキ商事株式会社コスモ・バイオ株式会社
Salutation			Country or Region *
Applicant Name *			Organization Name *
Department *
Email Address *			Product Name *
Cat. No.			Requested quantity *
Phone Number *
Remarks

Inhibitors & Agonists

Screening Libraries

Peptides

Name
Email *

	Sorry, but the email address you supplied was invalid.