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(I&PCI32765;&PCI 32765)
PCI-32765的分子结构式
PCI-32765(Ibrutinib)是Btk选择性抑制剂，IC50为0.5 nM，对Bmx，CSK，FGR，BRK，HCK有中度抑制性，但对EGFR，Yes， ErbB2，JAK3抑制性则较弱。
PCI-32765的价格及库存
10&mM&*&1&mL
MCE提供各种包装，敬请垂询。
PCI-32765的数据手册
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PCI-32765的其他形式产品
研究的其它产品
AVL-292 is a covalent, highly selective, orally active small molecule inhibitor of Btk with IC50 value of 0.5 nM; &1400-fold selectivity over the other kinases assayed. IC50 Value: & 0.5 nM [1] in vitro: AVL-292 forms a covalent bond with Cys481 in Btk and potently inhibits Btk in biochemical (IC50 & 0.5nM) and cellular assays (EC50 1-10 nM) including ?-IgM stimulation of BCR signaling, B cell proliferation and activation. Ramos cells were treated with AVL-292 for 1 hour followed by stimulation of the BCR with 5 ?g/mL ?-IgM for 10 minutes on ice.& Cell lysates were immunoblotted for Btk autophosphorylation (Y223), PLC?2 phosphorylation as well as activation of downstream Erk signaling.& AVL-292 inhibited Btk kinase activity in a cellular setting with EC50 between 1-10 nM [1]. in vivo: In healthy human subjects, AVL-292 was found to be safe and well tolerated following oral administration at dose levels ranging from 0.5-7.0 mg/kg.&& AVL-292 plasma levels and pharmacodynamic measurement of Btk engagement was dose-proportional across cohorts [1]. Subjects diagnosed with B cell malignancies received single daily oral doses of AVL-292 in continuous 28 day cycles. Total Btk content was determined in peripheral blood mononuclear cells at pre-dose, and Btk occupancy was determined 4 and 24 hours post dose on Day 1 and Day 28 [2]. Clinical trial: AVL-292 is currently being evaluated in a Phase 1b clinical trial in relapsed, refractory B cell malignancies including Chronic Lymphocytic Leukemia (CLL) and non-Hodgkin lymphomas. &
AVL-292 benzenesulfonate is a covalent, highly selective, orally active small molecule inhibitor of Btk with IC50 value of 0.5 nM; &1400-fold selectivity over the other kinases assayed. IC50 Value: & 0.5 nM [1] in vitro: AVL-292 forms a covalent bond with Cys481 in Btk and potently inhibits Btk in biochemical (IC50 & 0.5nM) and cellular assays (EC50 1-10 nM) including ?-IgM stimulation of BCR signaling, B cell proliferation and activation. Ramos cells were treated with AVL-292 for 1 hour followed by stimulation of the BCR with 5 ?g/mL ?-IgM for 10 minutes on ice.& Cell lysates were immunoblotted for Btk autophosphorylation (Y223), PLC?2 phosphorylation as well as activation of downstream Erk signaling.& AVL-292 inhibited Btk kinase activity in a cellular setting with EC50 between 1-10 nM [1]. in vivo: In healthy human subjects, AVL-292 was found to be safe and well tolerated following oral administration at dose levels ranging from 0.5-7.0 mg/kg.&& AVL-292 plasma levels and pharmacodynamic measurement of Btk engagement was dose-proportional across cohorts [1]. Subjects diagnosed with B cell malignancies received single daily oral doses of AVL-292 in continuous 28 day cycles. Total Btk content was determined in peripheral blood mononuclear cells at pre-dose, and Btk occupancy was determined 4 and 24 hours post dose on Day 1 and Day 28 [2]. Clinical trial: AVL-292 is currently being evaluated in a Phase 1b clinical trial in relapsed, refractory B cell malignancies including Chronic Lymphocytic Leukemia (CLL) and non-Hodgkin lymphomas. &
Btk inhibitor 1 is a& pyrazolo[3,4-d]pyrimidine derivative as a Btk kinase inhibitor. IC50 value: Target: Btk From PCT Int. Appl. (2012), WO
Btk inhibitor 1 Hcl is a& pyrazolo[3,4-d]pyrimidine derivative as a Btk kinase inhibitor. IC50 value: Target: Btk From PCT Int. Appl. (2012), WO
Btk inhibitor 1 R enantiomer is a& pyrazolo[3,4-d]pyrimidine derivative as a Btk kinase inhibitor. IC50 value: Target: Btk From PCT Int. Appl. (2012), WO
Btk inhibitor 1R enantiomer Hcl is a& pyrazolo[3,4-d]pyrimidine derivative as a Btk kinase inhibitor. IC50 value: Target: Btk From PCT Int. Appl. (2012), WO
CGI-1746 is a small-molecule Bruton's tyrosine kinase (Btk) inhibitor. IC50 value: Target: Btk CGI-1746 has exquisite selectivity for Btk and inhibits both auto- and transphosphorylation steps necessary for enzyme activation.& CGI-1746 is useful for heumatoid Arthritis
CNX-774 is a potent, selective, and orally available small molecule inhibitor of Btk (IC50& 1 nM) that forms a ligand-directed covalent bond with Cys-481, a non-conserved amino acid within the active site of the enzyme. IC50 Value: &1 nM [1] Target: Btk Kinase In biochemical assays, CNX-774 has demonstrated potent inhibition of Btk with an IC50 of &1nM in a continuous-read assay. The covalent bonding of CNX-774 to Btk was confirmed by incubating recombinant Btk protein with a 10-fold molar excess of CNX-774 for 1 hour at room temperature and analysis by MALDI-TOF MS.& A shift of protein mass corresponding to the molecular weight of CNX-774 confirmed the covalent bonding of CNX-774 to Btk.& Digestion of the covalently bonded Btk with pepsin followed by MSMS analysis established the bonding of CNX-774 to Cys-481.& Cellular potency as well as prolonged duration of action of CNX-774 was demonstrated in Ramos cells by using a biotinylated covalent probe that targets the same Cysteine residue as CNX-774. CNX-774 was found to be &90% extractable after 2 hrs of incubation in both rat and human whole blood.& These results demonstrate that CNX-774 has potent inhibitory activity towards the intended target, Btk, while achieving remarkable specificity in a variety of assays designed to assess off-target reactivity towards abundant cellular thiols and blood proteins. &
GDC-0834 is a potent and selective BTK inhibitor with in vitro IC50s of 5.9 and 6.4 nM in biochemical and cellular assays, respectively. IC50 value: 5.9 nM/6.4 nM(biochemical/cellular assay) [1] Target: BTK in vitro: GDC-0834 inhibited BTK with an in vitro IC(50) of 5.9 and 6.4 nM in biochemical and cellular assays, respectively, and in vivo IC(50) of 1.1 and 5.6 &M in mouse and rat, respectively [1]. in vivo: Administration of GDC- mg/kg) in a rat collagen-induced arthritis (CIA) model resulted in a dose-dependent decrease of ankle swelling and reduction of morphologic pathology [1]. GDC-0834 exhibited low clearance in PXB chimeric mice with humanized liver. Uncertainty in human pharmacokinetic prediction and high interest in a BTK inhibitor for clinical evaluation prompted an investigational new drug strategy, in which GDC-0834 was rapidly advanced to a single-dose human clinical trial. GDC-0834 plasma concentrations in humans were below the limit of quantitation (&1 ng/ml) in most samples from the cohorts dosed orally at 35 and 105 mg [2].
GDC-0834 Racemate is the racemate form of GDC-0834, which is a potent and selective BTK inhibitor with in vitro IC50s of 5.9 and 6.4 nM in biochemical and cellular assays, respectively. IC50 value: 5.9 nM/6.4 nM(biochemical/cellular assay) [1] Target: BTK in vitro: GDC-0834 inhibited BTK with an in vitro IC(50) of 5.9 and 6.4 nM in biochemical and cellular assays, respectively, and in vivo IC(50) of 1.1 and 5.6 &M in mouse and rat, respectively [1]. in vivo: Administration of GDC- mg/kg) in a rat collagen-induced arthritis (CIA) model resulted in a dose-dependent decrease of ankle swelling and reduction of morphologic pathology [1]. GDC-0834 exhibited low clearance in PXB chimeric mice with humanized liver. Uncertainty in human pharmacokinetic prediction and high interest in a BTK inhibitor for clinical evaluation prompted an investigational new drug strategy, in which GDC-0834 was rapidly advanced to a single-dose human clinical trial. GDC-0834 plasma concentrations in humans were below the limit of quantitation (&1 ng/ml) in most samples from the cohorts dosed orally at 35 and 105 mg [2].
PCI 29732 is a selective and irreversible Btk inhibitor with IC50 of 8.2 nM in a FRET based biochemical enzymology assay. IC50 value: 8.2 nM [1] Target: Btk kinase PCI 29732(compound 1) has a 8.2 nM potency against Btk in a FRET based biochemical enzymology assay. PCI 29732 shows only modest inhibitory activity against Itk, another Tec family kinase, probably due to the difference at the &gatekeeper& residue [1]. In human CD20+ B cells stimulated at the BCR, PCI-29732 blocked the transcriptional up-regulation of a panel of B-cell activation genes that occurs within 6 h of stimulation. Pulse exposure to the reversible inhibitor PCI-29732 did not result in BCR inhibition [2].
PCI-32765(Ibrutinib) racemate is a potent and highly selective Btk inhibitor with IC50 of 0.5 nM, modestly potent to Bmx, CSK, FGR, BRK, HCK, less potent to EGFR, Yes, ErbB2, JAK3, etc. IC50 value: 0.3 nM [1] Target: Btk in vitro: Ibrutinib shows the potent and irreversible inhibitory effect and selectivity for Btk enzymatic activity. In BCR pathway-activated DOHH2 cell line, Ibrutinib inhibits autophosphorylation of Btk, phosphorylation of Btk's physiological substrate PLC&, and phosphorylation of further downstream kinase, ERK with IC50 of 11 nM, 29 nM and 13 nM, respectively [1]. Ibrutinib exhibits a significant dose-dependent and time-dependent induction of cytotoxicity in chronic lymphocytic leukemia (CLL) cells. In addition, Ibrutinib induces cell death depending on caspase pathway activation and antagonizes the ability of CLL cells to proliferate after TLR signaling [2]. A recent study shows that Ibrutinib inhibits BCR-activated primary B cell proliferation with IC50 of 8 nM and results in inhibition of TNF&, IL-1& and IL-6 production in primary monocytes with IC50 of 2.6 nM, 0.5 nM and 3.9 nM, respectively [3]. in vivo: In a collagen-induced arthritis model, Ibrutinib significantly reduces clinical arthritis scores reflecting paw swelling and joint inflammation by inhibiting B-cell activation. In a MRL-Fas(lpr) lupus model, Ibrutinib reduces renal disease and autoantibody production [1]. In an adoptive transfer TCL1 mouse model of CLL, Ibrutinib (25 mg/kg/day) causes a transient early lymphocytosis, and delays CLL disease progression [4]. &
QL47 is a potent, selective and irreversible BTK kinase inhibitor with IC50 of 7 nM. IC50 Value: 7 nM Target: Btk in vitro: QL47 inhibits BTK kinase activity with an IC50 of 7 nM, inhibits autophosphorylation of BTK on Tyr223 in cells with an EC50 of 475 nM and inhibits phosphorylation of a downstream effector PLC&2 (Tyr759) with an EC50 of 318 nM. In Ramos cells QL47 induces a G1 cell cycle arrest which is associated with pronounced degradation of BTK protein. QL47 inhibits the proliferation of B-cell lymphoma cancer cell lines at submicromolar concentrations [1]. in vivo: N/A &
RN486 is a selective Btk inhibitor with an IC50 Value of 4.0 nM. IC50 Value: 4.0 nM [1] Target: Btk Kinase in vitro: In the enzymatic assay, the compound potently inhibited Btk kinase activity with an IC50 of 4.0 nM. RN486 not only potently and selectively inhibited the Btk enzyme, but also displayed functional activities in human cell-based assays in multiple cell types, blocking Fc& receptor cross-linking-induced degranulation in mast cells (IC(50) = 2.9 nM), Fc& receptor engagement-mediated tumor necrosis factor & production in monocytes (IC(50) = 7.0 nM), and B cell antigen receptor-induced expression of an activation marker, CD69, in B cells in whole blood (IC(50) = 21.0 nM) [1].& In a co-culture system consisting of human primary synovial FLS and activated human platelets, convulxin stimulation resulted in elevated production of pro-inflammatory cytokines, IL-6 and IL-8, an effect which was dose-dependently blocked by RN486 [2]. in vivo: RN486 displayed similar functional activities in rodent models, effectively preventing type I and type III hypersensitivity responses. More importantly, RN486 produced robust anti-inflammatory and bone-protective effects in mouse CIA and rat adjuvant-induced arthritis (AIA) models. In the AIA model, RN486 inhibited both joint and systemic inflammation either alone or in combination with methotrexate, reducing both paw swelling and inflammatory markers in the blood [1]. The administration of RN486 completely stopped disease progression, as determined by histologic and functional analyses of glomerular nephritis. The efficacy was associated with striking inhibition of B cell activation, as demonstrated by a significant reduction in CD69 expression in response to BCR crosslinking. RN486 markedly reduced the secretion of IgG anti-double-stranded DNA (anti-dsDNA) secretion, as determined by enzyme-linked immunosorbent and enzyme-linked immunospot assays [3]. &
PCI-32765的生物活性
PCI-32765(Ibrutinib) is a potent and highly selective Btk inhibitor with IC50 of 0.5 nM, modestly potent to Bmx, CSK, FGR, BRK, HCK, less potent to EGFR, Yes, ErbB2, JAK3, etc. IC50 value: 0.3 nM Target: Btk in vitro: Ibrutinib shows the potent and irreversible inhibitory effect and selectivity for Btk enzymatic activity. In BCR pathway-activated DOHH2 cell line, Ibrutinib inhibits autophosphorylation of Btk, phosphorylation of Btk's physiological substrate PLC&, and phosphorylation of further downstream kinase, ERK with IC50 of 11 nM, 29 nM and 13 nM, respectively [1]. Ibrutinib exhibits a significant dose-dependent and time-dependent induction of cytotoxicity in chronic lymphocytic leukemia (CLL) cells. In addition, Ibrutinib induces cell death depending on caspase pathway activation and antagonizes the ability of CLL cells to proliferate after TLR signaling [2]. A recent study shows that Ibrutinib inhibits BCR-activated primary B cell proliferation with IC50 of 8 nM and results in inhibition of TNF&, IL-1& and IL-6 production in primary monocytes with IC50 of 2.6 nM, 0.5 nM and 3.9 nM, respectively [3]. in vivo: In a collagen-induced arthritis model, Ibrutinib significantly reduces clinical arthritis scores reflecting paw swelling and joint inflammation by inhibiting B-cell activation. In a MRL-Fas(lpr) lupus model, Ibrutinib reduces renal disease and autoantibody production [1]. In an adoptive transfer TCL1 mouse model of CLL, Ibrutinib (25 mg/kg/day) causes a transient early lymphocytosis, and delays CLL disease progression [4]. &
参考CoA中推荐的条件进行储存。
C25H24N6O2
溶剂/溶解度
DMSO &85mg/mL Water &1.2mg/mL Ethanol &1.8mg/mL
[1]. [2]. [3]. [4].503 Service Temporarily Unavailable
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