Anticancer 99% Purity Ibrutinib Pharmaceutical Intermediate Ibrutinib Powder Ibrutinib
China Anticancer 99% Purity Ibrutinib Pharmaceutical Intermediate Ibrutinib Powder Ibrutinib, Find details about China Ibrutinib, Supply Ibrutinib from Anticancer 99% Purity Ibrutinib Pharmaceutical Intermediate Ibrutinib Powder Ibrutinib
Basic Info.
Model NO.
D-sung Ibrutinib
Product Name
Ibrutinib
Name
Ibrutinib Powder
Appearance
White Powder
Color
White
Grade
Pharmaceutical Grade
Assay
HPLC 99%
Application
Anticancer
Specific
COA
Test Method
HPLC
Shelf Life
2 Years
CAS No.
936563-96-1
Mf
C25h24n6o2
MW
440.507
Melting Point
149-158oc
Density
1.34
Trademark
D-sung
Transport Package
Negotiable
Specification
99%
Origin
Shaanxi Xi′an
Model NO.
D-sung Ibrutinib
Product Name
Ibrutinib
Name
Ibrutinib Powder
Appearance
White Powder
Color
White
Grade
Pharmaceutical Grade
Assay
HPLC 99%
Application
Anticancer
Specific
COA
Test Method
HPLC
Shelf Life
2 Years
CAS No.
936563-96-1
Mf
C25h24n6o2
MW
440.507
Melting Point
149-158oc
Density
1.34
Trademark
D-sung
Transport Package
Negotiable
Specification
99%
Origin
Shaanxi Xi′an
Product Desciption
Anticancer 99% Purity Ibrutinib Pharmaceutical Intermediate Ibrutinib Powder Ibrutinib
| Product name | Ibrutinib |
| Cas number | 936563-96-1 |
| Apperance | White powder |
| MF | C25H24N6O2 |
| MW | 440.507 |
Ibrutinib, a targeted anticarcinogenesis drug developed by Johnson Johnson and Pharmacyclics Inc., was approved by the U.S. Food and Drug Administration (FDA) on November 13, 2013.The drug, marketed under the trade name Imbruvica, is used for the treatment of mantle cell lymphoma (MCL).
Ibrutinib is a highly selective Bruton's tyrosine kinase (Btk) irreversible inhibitor.PCI-32765 (Ibrutinib) is a selective and irreversible pyrrolopyrimidine-based inhibitor of BTK with IC50 of 0.5 nM. [1] PCI-32765 binds irreversibly to Cys-481 in BTK and thus is only active with other kinases with such a modifiable cysteine residue. In DOHH2 cells, in which the BCR pathway can be activated by anti-IgG, PCI-32765 inhibits autophosphorylation of BTK (IC50, 11 nM), BTK's physiological substrate, PLCg (IC50, 29 nm), and downstream ERK (IC50, 13 nm).
PCI-32765 (Ibrutinib) may be an important new targeted treatment approach for CLL pts. In ex vivo assays with whole bold, PCI-32765 (Ibrutinib) prevents the activation of human BCR with an IC50 of about 0.2 μM, while not influencing the activation of T cell. Treatment of CD40 or BCR activated CLL cells with PCI-32765 (Ibrutinib) results in inhibition of BTK tyrosine phosphorylation and also effectively abrogates downstream survival pathways activated by this kinase including ERK1/2, PI3K, and NF-κB. In addition, PCI-32765 (Ibrutinib) prevents activation-induced proliferation of CLL cells in vitro, and effectively inhibits survival signals provided externally to CLL cells from the microenvironment including soluble factors (CD40L, BAFF, IL-6, IL-4, and TNF-α), fibronectin engagement, and stromal cell contact. PCI-32765 is originally developed by Pharmacyclics. And participants is been invited for the phase I clinical trials.
Ibrutinib is a highly selective Bruton's tyrosine kinase (Btk) irreversible inhibitor.PCI-32765 (Ibrutinib) is a selective and irreversible pyrrolopyrimidine-based inhibitor of BTK with IC50 of 0.5 nM. [1] PCI-32765 binds irreversibly to Cys-481 in BTK and thus is only active with other kinases with such a modifiable cysteine residue. In DOHH2 cells, in which the BCR pathway can be activated by anti-IgG, PCI-32765 inhibits autophosphorylation of BTK (IC50, 11 nM), BTK's physiological substrate, PLCg (IC50, 29 nm), and downstream ERK (IC50, 13 nm). PCI-32765 (Ibrutinib) may be an important new targeted treatment approach for CLL pts. In ex vivo assays with whole bold, PCI-32765 (Ibrutinib) prevents the activation of human BCR with an IC50 of about 0.2 μM, while not influencing the activation of T cell. Treatment of CD40 or BCR activated CLL cells with PCI-32765 (Ibrutinib) results in inhibition of BTK tyrosine phosphorylation and also effectively abrogates downstream survival pathways activated by this kinase including ERK1/2, PI3K, and NF-κB. In addition, PCI-32765 (Ibrutinib) prevents activation-induced proliferation of CLL cells in vitro, and effectively inhibits survival signals provided externally to CLL cells from the microenvironment including soluble factors (CD40L, BAFF, IL-6, IL-4, and TNF-α), fibronectin engagement, and stromal cell contact. PCI-32765 is originally developed by Pharmacyclics. And participants is been invited for the phase I clinical trials.
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