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Results for "

intracranial

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Acyltransferase (1) Dopamine Transporter (1) EGFR (1) NF-κB (1) Raf (1)
By Research Areas:	Cancer (3) Metabolic Disease (1) Neurological Disease (6)

Inhibitors & Agonists

Fluorescent Dye

Peptides

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-153268

BDTX-1535 EGFR-IN-76	EGFR	Cancer
BDTX-1535 (EGFR-IN-76, compound 37A) is an orally active, brain-penetrant, selective and potent EGFR tyrosine kinase inhibitor. BDTX-1535 achieves potent anti-tumor activity against EGFR alterations and amplification across models including NSCLC, GBM PDX and intracranial tumors .

HY-117656

ESI-05 3 Publications Verification NSC 116966	Acyltransferase	Neurological Disease Metabolic Disease
ESI-05 is a specific exchange proteins directly activated by cAMP 2 (EPAC2) inhibitor. ESI-05 inhibits cAMP-mediated EPAC2 GEF activity with an IC₅₀ of 0.43 μM. ESI-05 can be used for the research of diabetes, insulin secretion and neurological disorders .

HY-150639

Everafenib	Raf	Cancer
Everafenib is a potent and blood-brain barrier (BBB) penetrant BRAF inhibitor, also inhibits MAPK signaling. Everafenib has inhibitory activity against a panel of ^V600EBRAF melanoma cell lines with IC₅₀ values of 2-10 nM, which is better than Dabrafenib (HY-14660) and Vemurafenib (HY-12057). Everafenib has efficacy in an intracranial mouse model of metastatic melanoma .

HY-117902

SRI-31142	Dopamine Transporter	Neurological Disease
SRI-31142 is a putative, brain-penetrant allosteric inhibitor of the dopamine transporter (DAT). In behavioral studies using intracranial self-stimulation (ICSS), SRI-31142 did not produce the abuse-related effects seen with cocaine and GBR-12935, but instead reduced ICSS responses and dopamine levels in the nucleus accumbens (NAc) at effective doses. SRI-31142 also blocked cocaine-induced increases in ICSS and NAc dopamine .

HY-149696

IR-Crizotinib	NF-κB	Cancer
IR-Crizotinib is a NF-κB-inducing kinase (NIK) inhibitor that crosses the blood-brain barrier and fluorescently localizes intracranial glioblastoma (GBM) in mice (IC₅₀=3.381 μM). IR-Crizotinib is conjugated from the near-infrared dye IR-786 and the NF-κB-inducing kinase (NIK) inhibitor Crizotinib. IR-Crizotinib can effectively inhibit the growth and invasion of glioma in vitro and in vivo and can be used in cancer research .

Cat. No.	Product Name	Type

HY-149696

IR-Crizotinib	Dyes
IR-Crizotinib is a NF-κB-inducing kinase (NIK) inhibitor that crosses the blood-brain barrier and fluorescently localizes intracranial glioblastoma (GBM) in mice (IC₅₀=3.381 μM). IR-Crizotinib is conjugated from the near-infrared dye IR-786 and the NF-κB-inducing kinase (NIK) inhibitor Crizotinib. IR-Crizotinib can effectively inhibit the growth and invasion of glioma in vitro and in vivo and can be used in cancer research .

IR-Crizotinib

Dyes

IR-Crizotinib is a NF-κB-inducing kinase (NIK) inhibitor that crosses the blood-brain barrier and fluorescently localizes intracranial glioblastoma (GBM) in mice (IC₅₀=3.381 μM). IR-Crizotinib is conjugated from the near-infrared dye IR-786 and the NF-κB-inducing kinase (NIK) inhibitor Crizotinib. IR-Crizotinib can effectively inhibit the growth and invasion of glioma in vitro and in vivo and can be used in cancer research .

Cat. No.	Product Name	Target	Research Area

HY-P5118A

Tat-peptide 190-208 TFA	Peptides	Neurological Disease
Tat-peptide 190-208 TFA is a cell-permeable and Tat-labeled fusion peptide, corresponding to residues 190-208 of rat G3BP1. Tat sequence from HIV, is placed at the least conserved end of the sequence, for cell permeability. Tat-peptide 190-208 TFA increases axon growth and increases the number of neurites per neuron. Tat-peptide 190-208 TFA likely exhibits an axon intrinsic mechanism. Tat-peptide 190-208 TFA can be used for ischemic protection during endovascular repair for intracranial aneurysms .

HY-P5118

Tat-peptide 190-208	Peptides	Neurological Disease
Tat-peptide 190-208 is a cell-permeable and Tat-labeled fusion peptide, corresponding to residues 190-208 of rat G3BP1. Tat sequence from HIV, is placed at the least conserved end of the sequence, for cell permeability. Tat-peptide 190-208 increases axon growth and increases the number of neurites per neuron. Tat-peptide 190-208 likely exhibits an axon intrinsic mechanism. Tat-peptide 190-208 can be used for ischemic protection during endovascular repair for intracranial aneurysms .

HY-P5119

Tat-peptide control 168-189	Peptides	Neurological Disease
Tat-peptide 168-189 is a cell-permeable and Tat-labeled fusion peptide, corresponding to residues 168-189 of rat G3BP1. Tat sequence from HIV, is placed at the least conserved end of the sequence, for cell permeability. Tat-peptide 168-189 is the negtive control of Tat-peptide 190-208 (HY-P5118), as Tat-peptide 190-208 increases axon growth and increases the number of neurites per neuron .

HY-P5119A

Tat-peptide control 168-189 TFA	Peptides	Neurological Disease
Tat-peptide 168-189 is a cell-permeable and Tat-labeled fusion peptide, corresponding to residues 168-189 of rat G3BP1. Tat sequence from HIV, is placed at the least conserved end of the sequence, for cell permeability. Tat-peptide 168-189 is the negtive control of Tat-peptide 168-189 TFA (HY-P5118A), as Tat-peptide 168-189 TFA increases axon growth and increases the number of neurites per neuron .

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