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Idelalisib/艾代拉里斯 {[allProObj[0].p_purity_real_show]}

货号:A134749 同义名: CAL-101; GS-1101

Idelalisib(CAL-101;GS-1101)是一种高度选择性且口服生物利用度的p110δ抑制剂,IC50为2.5 nM,相对于其他I类PI3K酶展示了40至300倍的选择性。

Idelalisib/艾代拉里斯 化学结构 CAS号:870281-82-6
Idelalisib/艾代拉里斯 化学结构
CAS号:870281-82-6
Idelalisib/艾代拉里斯 3D分子结构
CAS号:870281-82-6
Idelalisib/艾代拉里斯 化学结构 CAS号:870281-82-6
Idelalisib/艾代拉里斯 3D分子结构 CAS号:870281-82-6
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Idelalisib/艾代拉里斯 纯度/质量文件 产品仅供科研

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产品名称 C2β p110α p110β p110γ p110δ PI3K Vps34 其他靶点 纯度
A66 +

C2β, IC50: 462 nM

++

p110α, IC50: 32 nM

99%+
Taselisib +

C2β, IC50: 292 nM

++++

PI3Kα, Ki: 0.29 nM

+++

PI3Kβ, Ki: 9.1 nM

++++

PI3Kγ, Ki: 0.97 nM

++++

PI3Kδ, Ki: 0.12 nM

+

hVps34, IC50: 374 nM

99%+
Gedatolisib ++++

PI3Kα, IC50: 0.4 nM

+++

PI3Kγ, IC50: 5.4 nM

mTOR 99%
HS-173 ++++

PI3Kα , IC50: 0.8 nM

99%+
Serabelisib +++

PI3Kα, IC50: 21 nM

99%+
GNE-477 ++++

PI3Kα, IC50: 4 nM

mTOR 99%
YM-201636 +

p110α, IC50: 3.3 μM

PIKfyve 98%
AS-252424 +

PI3Kα, IC50: 935 nM

++

PI3Kγ, IC50: 33 nM

99%
Alpelisib +++

PI3Kα, IC50: 5 nM

99%+
AS-604850 +

PI3Kα, IC50: 4.5 μM

+

PI3Kγ, IC50: 0.25 μM

99%
SF2523 ++

PI3Kα, IC50: 34 nM

++

PI3Kγ, IC50: 158 nM

mTOR,DNA-PK 99%+
Inavolisib ++++

PI3K alpha, IC50: 0.038 nM

99%+
Bimiralisib ++++

PI3Kα, Kd: 1.5 nM

+++

PI3Kβ, Kd: 11 nM

++

PI3Kγ, Kd: 25 nM

++

PI3Kδ, Kd: 25 nM

mTOR 99%+
GSK1059615 ++++

PI3Kα, IC50: 0.4 nM

++++

PI3Kβ, IC50: 0.6 nM

+++

PI3Kγ, IC50: 5 nM

++++

PI3Kδ, IC50: 2 nM

mTOR 98%
GSK2636771 99%
Fimepinostat +++

PI3Kα, IC50: 19 nM

++

PI3Kβ, IC50: 54 nM

++

PI3Kδ, IC50: 39 nM

99%+
VS-5584 ++++

PI3Kα, IC50: 2.6 nM

+++

PI3Kβ, IC50: 21 nM

++++

PI3Kγ, IC50: 3.0 nM

++++

PI3Kδ, IC50: 2.7 nM

mTOR 98%
Dactolisib ++++

p110α1, IC50: 4 nM

++

p110β, IC50: 75 nM

+++

p110γ, IC50: 5 nM

+++

p110δ, IC50: 7 nM

98+%
PI-103 ++++

p110α, IC50: 2 nM

++++

p110β, IC50: 3 nM

+++

p110γ, IC50: 15 nM

++++

p110δ, IC50: 3 nM

mTOR,DNA-PK 99%+
PI-3065 +

p110β, IC50: 1078 nM

+++

p110δ, IC50: 15 nM

99%+
Voxtalisib ++

PI3Kα, IC50: 39 nM

++

PI3Kβ, IC50: 113 nM

+++

PI3Kγ, IC50: 9 nM

++

PI3Kδ, IC50: 43 nM

mTOR,DNA-PK 99%+
AZD-8835 +++

PI3Kα, IC50: 6.2 nM

+

PI3Kβ, IC50: 431 nM

++

PI3Kγ, IC50: 90 nM

+++

PI3Kδ, IC50: 5.7 nM

99%
Pilaralisib analogue ++

PI3Kα, IC50: 39 nM

++

PI3Kβ, IC50: 36 nM

+++

PI3Kγ, IC50: 23 nM

++

PI3Kδ, IC50: 36 nM

99%+
ZSTK474 +++

PI3Kα, IC50: 16 nM

++

PI3Kβ, IC50: 44 nM

++

PI3Kγ, IC50: 49 nM

+++

PI3Kδ, IC50: 4.6 nM

++

PI3K, IC50: 37 nM

98%
AS-605240 ++

PI3Kα, IC50: 60 nM

+

PI3Kβ, IC50: 270 nM

+++

PI3Kγ, IC50: 8 nM

+

PI3Kδ, IC50: 300 nM

98%
TGX-221 +++

p110β, IC50: 5 nM

++

p110δ, IC50: 0.1 μM

99%+
PF-04691502 ++++

PI3Kα, Ki: 1.8 nM

++++

PI3Kβ, Ki: 2.1 nM

++++

PI3Kγ, Ki: 1.9 nM

++++

PI3Kδ, Ki: 1.6 nM

mTOR 98+%
GDC-0084 ++++

PI3Kα, Ki app: 2 nM

++

PI3Kβ, Ki app: 46 nM

+++

PI3Kγ, Ki app: 10 nM

++++

PI3Kδ, Ki app: 3 nM

mTOR 99%+
Buparlisib ++

p110α, IC50: 52 nM

+

p110β, IC50: 166 nM

+

p110γ, IC50: 262 nM

++

p110δ, IC50: 116 nM

+

Vps34, IC50: 2.4 μM

mTOR 98%
LY294002 +

p110α, IC50: 0.5 μM

+

p110β, IC50: 0.97 μM

+

p110δ, IC50: 0.57 μM

DNA-PK 99%+
AZD 6482 +

PI3Kα, IC50: 870 nM

+++

PI3Kβ, IC50: 10 nM

++

PI3Kδ, IC50: 80 nM

DNA-PK 99%+
Pictilisib ++++

p110α, IC50: 3 nM

++

p110β, IC50: 33 nM

++

p110γ, IC50: 75 nM

++++

p110δ, IC50: 3 nM

mTOR 99%+
PKI-402 ++++

PI3Kα, IC50: 2 nM

+++

PI3Kβ, IC50: 7 nM

+++

PI3Kγ, IC50: 16 nM

+++

PI3Kδ, IC50: 14 nM

mTOR 98%
Copanlisib ++++

PI3Kα, IC50: 0.5 nM

++++

PI3Kβ, IC50: 3.7 nM

+++

PI3Kγ, IC50: 6.4 nM

++++

PI3Kδ, IC50: 0.7 nM

99%+
Omipalisib ++++

p110α, Ki: 0.019 nM

++++

p110β, Ki: 0.13 nM

++++

p110γ, Ki: 0.06 nM

++++

p110δ, Ki: 0.024 nM

99%+
Izorlisib +++

PI3Kα, IC50: 14 nM

++

PI3Kβ, IC50: 0.12 μM

++

PI3Kγ, IC50: 36 nM

+

PI3Kδ, IC50: 0.50 μM

99%+
AZD8186 ++

PI3Kα, IC50: 35 nM

++++

PI3Kβ, IC50: 4 nM

+++

PI3Kδ, IC50: 12 nM

99%
KU-0060648 ++++

PI3Kα, IC50: 4 nM

++++

PI3Kβ, IC50: 0.5 nM

+

PI3Kγ, IC50: 0.59 μM

++++

PI3Kδ, IC50: 0.1 nM

DNA-PK 98%
Apitolisib +++

p110α, IC50: 5 nM

++

p110β, IC50: 27 nM

+++

p110γ, IC50: 14 nM

+++

p110δ, IC50: 7 nM

mTOR 98%+
CZC24832 +

PI3Kβ, IC50: 1.1 μM

++

PI3Kγ, IC50: 27 nM

98+%
BGT226 maleate ++++

PI3Kα, IC50: 4 nM

++

PI3Kβ, IC50: 63 nM

++

PI3Kγ, IC50: 38 nM

mTOR 99%+
TG 100713 ++

PI3Kα, IC50: 165 nM

+

PI3Kβ, IC50: 215 nM

++

PI3Kγ, IC50: 50 nM

+++

PI3Kδ, IC50: 24 nM

98%+
PI3K-IN-1 ++

PI3Kα, IC50: 39 nM

++

PI3Kβ, IC50: 113 nM

+++

PI3Kγ, IC50: 9 nM

++

PI3Kδ, IC50: 43 nM

mTOR,DNA-PK 98+%
TG100-115 +

PI3Kα, IC50: 1.3 μM

+

PI3Kβ, IC50: 1.2 μM

++

PI3Kγ, IC50: 83 nM

+

PI3Kδ, IC50: 235 nM

98%
PIK-90 +++

PI3Kα, IC50: 11 nM

+

PI3Kβ, IC50: 350 nM

+++

PI3Kγ, IC50: 18 nM

++

PI3Kδ, IC50: 58 nM

99%+
PIK-294 +

p110β, IC50: 490 nM

++

p110γ, IC50: 160 nM

+++

p110δ, IC50: 10 nM

99%+
Duvelisib ++++

PI3Kβ, Ki: 1564 pM

++

PI3Kγ, Ki: 243 pM

++++

PI3Kδ, Ki: 23 pM

99%+
GDC-0326 ++++

PI3Kα, Ki: 0.2 nM

++

PI3Kβ, Ki: 26.6 nM

+++

PI3Kγ, Ki: 10.2 nM

++++

PI3Kδ, Ki: 4 nM

98%
Quercetin Dihydrate +

PI3Kβ, IC50: 5.4 μM

+

PI3Kγ, IC50: 2.4 μM

+

PI3Kδ, IC50: 3.0 μM

95%
Quercetin +

PI3Kβ, IC50: 5.4 μM

+

PI3Kγ, IC50: 2.4 μM

+

PI3Kδ, IC50: 3.0 μM

Src,Sirtuin,PKC 95%
Leniolisib +

PI3Kα, IC50: 0.244 μM

+

PI3Kβ, IC50: 0.424 μM

+

PI3Kγ, IC50: 2.23 μM

+++

PI3Kδ, IC50: 0.011 μM

DNA-PK 99%+
PIK-108 99%
Eganelisib +++

PI3Kγ, IC50: 16 nM

99%+
CAY10505 99%
IPI-3063 ++++

p110δ, IC50: 2.5 nM

99%
Nemiralisib ++++

PI3Kδ, pKi: 9.9

99%+
PF-4989216 ++++

p110α, IC50: 2 nM

++

p110γ, IC50: 65 nM

++++

p110δ, IC50: 1 nM

99%+
PIK-75 HCl +++

p110α, IC50: 5.8 nM

++

p110γ, IC50: 76 nM

+

p110δ, IC50: 0.51 μM

DNA-PK 99%+
Tenalisib ++

PI3Kγ, IC50: 33.2 nM

++

PI3Kδ, IC50: 24.5 nM

98%
Acalisib +++

p110δ, IC50: 14 nM

99%+
Umbralisib +++

PI3Kδ, IC50: 22.2 nM

99%+
AMG319 +

PI3Kγ, IC50: 850 nM

+++

PI3Kδ, IC50: 18 nM

99%
IC-87114 +

PI3Kγ, IC50: 29 μM

+

PI3Kδ, IC50: 0.5 μM

99%+
Idelalisib ++

p110γ, IC50: 89 nM

++++

p110δ, IC50: 2.5 nM

98%
PIK-293 +

p110γ, IC50: 10 μM

+

p110δ, IC50: 0.24 μM

99%+
Vps34-PIK-III +

PI3Kδ, IC50: 1.2μM

+++

Vps34, IC50: 0.018μM

99%+
GSK2292767 98%
Seletalisib +

PI3Kγ, IC50: 282 nM

+++

PI3Kδ, IC50: 12 nM

99%+
P110δ-IN-1 ++++

P110δ, IC50: 0.6 nM

99%
PI3Kδ-IN-5 ++++

PI3Kδ, IC50: 0.9 nM

99%
SRX3207 +

PI3K alpha, IC50: 244 nM

+

PI3K gamma, IC50: 9790 nM

+

PI3K delta, IC50: 388 nM

Syk 98%
Parsaclisib HCl ++++

PI3Kδ, IC50: 1 nM

98%
IHMT-PI3Kδ-372 +++

PI3Kδ, IC50: 14 nM

98%
Trigonelline Akt 99%+
Wortmannin ++++

PI3K, IC50: 3 nM

MLCK,DNA-PK 99%+
Samotolisib DNA-PK 99%+
GNE-317 99%+
Oroxin B Akt,PTEN 99%+
NU 7026 +

PI3K, IC50: 13 μM

DNA-PK 98+%
Deguelin Akt 99%+
Ailanthone Akt,ATM/ATR,CDK 98%
Resibufogenin ROS 98%
KU-57788 +

PI3K, IC50: 5 μM

mTOR,DNA-PK 99%+
Cinobufagine Akt 99%
α-Linolenic acid 97% (GC)
MTX-211 EGFR 98%
PI3K/mTOR Inhibitor-2 ++++

PI3K, IC50: 3.4 nM

mTOR 99%+
SPP-86 99%+
(E)-Akt inhibitor-IV 98%
Vps34-IN-1 ++

Vps34, IC50: 25 nM

98%
SAR405 ++++

Vps34, IC50: 1.2 nM

98+%
3-Methyladenine +

PI3Kγ, IC50: 60 μM

+

Vps34, IC50: 25 μM

Autophagy 98%
Vps34-IN-4 +++

VPS34, IC50: 15 nM

98%+
Autophinib +++

Vps34, IC50: 19 nM

Autophagy 99%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。

Idelalisib/艾代拉里斯 生物活性

靶点
  • p110γ

    p110γ, IC50:89 nM

  • p110δ

    p110δ, IC50:2.5 nM

描述 PI3Ks are lipid kinases participating in several cellular process. There are eight PI3Ks, which have been identified as classes IA, 1B, II and III based on the sequence homology and substrate preference. The class IA PI3K is a heterodimer consisting of a 110 kDa catalytic subunit (p110α, p110β and p110δ), and an 85 kDa regulatory subunit[2]. CAL-101 is an orally available and selective inhibitor of p110δ (IC50=2.5nM, analyzed using the SelectScreen kinase inhibitor assay service) with less potent to p110γ (IC50=89nM). In SU-DHL-5, KARPAS-422 and B-ALL (CCRF-SB) cell lines, CAL-101 can produce a concentration-dependent reduction in pAktS473, pAktT308 and the downstream target S6 and also induce apoptosis significantly[1]. It has also been found that CAL-101 can induce caspase-dependent death of malignant CLL cells, suppresse the production of protumor cytokine by T and NK cells, as well as abrogate prosurvival microenvironmental signals like B-cell activating factor, tumor necrosis factor and fibronectin[3]. Thus, CAL-101 has effects both on tumor microenvironment and directly on tumors. Now CAL-101 has been used in monotherapy studies in patients with non-Hodgkin lymphoma (Phase1/2)[4].
作用机制 Idelalisib can bind to the ATP-binding pocket of PI3Kδ, which is responsible for the selectivity for PI3Kδ.[5]

Idelalisib/艾代拉里斯 细胞实验

Cell Line
Concentration Treated Time Description References
Maver-1 1 μM 8 hours To analyze the effect of combination therapy on gene expression in Maver-1 cells. Results showed that combination therapy significantly altered the gene expression profile. Acta Pharmacol Sin. 2022 Feb;43(2):457-469
Z-138 2 μM 96 hours To evaluate the effect of A-485 combined with idelalisib on the proliferation of Z-138 cells. Results showed that A-485 significantly enhanced the sensitivity to idelalisib. Acta Pharmacol Sin. 2022 Feb;43(2):457-469
SUM159 25 μM 96 h To test the growth inhibitory effect of Idelalisib on TNBC cells Breast Cancer Res. 2019 Feb 1;21(1):20.
BT549 25 μM 96 h To test the growth inhibitory effect of Idelalisib on TNBC cells Breast Cancer Res. 2019 Feb 1;21(1):20.
murine thymocytes 10 µM To investigate the effect of Idelalisib on thymocyte respiration, results showed that Idelalisib had no significant effect on thymocyte respiration Exp Hematol Oncol. 2016 Jul 29;5:22.
HCT-116 cells 10 μM 48 h Inhibition of PIK3CD significantly suppressed the growth, migration, and invasion of HCT-116 cells. Cancer Sci. 2019 Mar;110(3):997-1011.
Huh-BAT 20 μM 48 h Suppressed HCC cell proliferation and induced cell cycle arrest, reduced cell invasion, upregulated E-cadherin expression, and downregulated N-cadherin and Snail expression. Clin Mol Hepatol. 2020 Oct;26(4):529-539.
HepG2 20 μM 48 h Suppressed HCC cell proliferation and induced cell cycle arrest, reduced cell invasion, upregulated E-cadherin expression, and downregulated N-cadherin and Snail expression. Clin Mol Hepatol. 2020 Oct;26(4):529-539.
MEC1 cells 2 μM 5 days To investigate the effect of Idelalisib on Rictor and pAktS473 levels in MEC1 cells, results showed upregulation of Rictor and pAktS473 levels. J Clin Invest. 2024 Oct 22;134(23):e173770.
CLL cells 1 μM 48 h To investigate the effect of Idelalisib on Akt phosphorylation in CLL cells, results showed inhibition of Akt phosphorylation. J Clin Invest. 2024 Oct 22;134(23):e173770.
Human platelets 10 µM 10 min To evaluate the inhibitory effect of PI3K inhibitors on intracellular calcium release induced by the GPVI-specific agonist CRP, results showed that Idelalisib significantly inhibited calcium release. Int J Mol Sci. 2021 Mar 24;22(7):3304.
Human platelets 10 µM 10 min To assess the potential toxicity of Idelalisib on platelet viability using Calcein-AM flow cytometry, results showed that platelets remained highly viable after Idelalisib treatment. Int J Mol Sci. 2021 Mar 24;22(7):3304.

Idelalisib/艾代拉里斯 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Mice C57BL/6 mice Intraperitoneal injection 2.5 µg/g Once daily for 4 days To investigate the effect of Idelalisib on thymus size, results showed that Idelalisib had no significant effect on thymus size Exp Hematol Oncol. 2016 Jul 29;5:22.
Nude mice HCT-116 xenograft model Oral 30 mg/kg/d Once daily for 10 days Inhibition of PIK3CD significantly suppressed the growth of HCT-116 xenograft tumors. Cancer Sci. 2019 Mar;110(3):997-1011.
Mice ITK-SYKCD4-CreERT2;PD-1-/- mice Oral 10 mg/kg 5 days a week for 5 days To study the effect of PI3K inhibition on ITK-SYK+PD-1-/- lymphoma mice, results showed that PI3K inhibition significantly extended the lifespan of these mice. Nature. 2017 Dec 7;552(7683):121-125
Mice FeCl3-induced arterial thrombosis model Oral administration 20 mg/kg Single dose, experiments performed 1 hour after administration To evaluate the antithrombotic effect of Idelalisib in the FeCl3-induced arterial thrombosis model, results showed that Idelalisib significantly prolonged the occlusion time, indicating its antithrombotic potential. Int J Mol Sci. 2021 Mar 24;22(7):3304.
Nude mice HCT 116 xenograft model Intragastric administration 15 mg/kg Once daily for 21 days To evaluate the antitumor effect of Idelalisib in vivo on KRAS-mutant colorectal cancer, the results showed that Idelalisib significantly inhibited tumor growth without obvious hepatotoxicity or renal toxicity. Cell Death Dis. 2024 Jul 3;15(7):474

Idelalisib/艾代拉里斯 动物研究

Dose Mice: min = 10 mg/kg[6], max = 40 mg/kg[7]
Administration p.o, i.v, i.p

Idelalisib/艾代拉里斯 临床研究

NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT03310190 - Recruiting June 15, 2020 Canada, Alberta ... 展开 >> University of Calgary /ID# 166416 Recruiting Calgary, Alberta, Canada, T2N 4Z6 Cross Cancer Institute /ID# 166417 Not yet recruiting Edmonton, Alberta, Canada, T6G 1Z2 Canada, New Brunswick The Moncton Hospital /ID# 166043 Recruiting Moncton, New Brunswick, Canada, E1C 6Z8 Saint John Regional Hospital /ID# 202190 Not yet recruiting Saint John, New Brunswick, Canada, E2L 4L2 Canada, Ontario William Osler Health System /ID# 202049 Not yet recruiting Brampton, Ontario, Canada, L6R 3J7 Michael Garron Hospital/Toronto East Health Network /ID# 209463 Not yet recruiting East York, Ontario, Canada, M4C 3E7 Kingston Health Sciences Centr /ID# 169252 Recruiting Kingston, Ontario, Canada, K7L 2V7 The Ottawa Hospital Research /ID# 166041 Recruiting Ottawa, Ontario, Canada, K1H 8L6 Health Sciences North /ID# 205817 Recruiting Sudbury, Ontario, Canada, P3N 1H5 Canada, Quebec Jewish General Hospital /ID# 166418 Recruiting Montreal, Quebec, Canada, H3T 1E2 Cisss Du Bas-Saint-Laurent Hopital Regional de Rimouski /Id# 201202 Recruiting Rimouski, Quebec, Canada, G5L 5T1 Canada CancerCare Manitoba /ID# 170751 Recruiting Manitoba, Canada, R3E 0V9 Thunder Bay Regional Health Re /ID# 204740 Not yet recruiting Thunder Bay, Canada, P7B 6V4 收起 <<
NCT03283137 CLL B-cell No... 展开 >>n Hodgkin Lymphoma 收起 << Phase 1 Recruiting December 2020 United States, Illinois ... 展开 >> University of Chicago Recruiting Chicago, Illinois, United States, 60637 Contact: Michael Thirman, MD       mthirman@medicine.bsd.uchicago.edu    Contact: Howard Weiner    7737022084    hweiner@medicine.bsd.uchicago.edu 收起 <<
NCT02141282 Chronic Lymphocytic Leukemia Phase 2 Active, not recruiting December 8, 2021 United States, California ... 展开 >> Ucsd /Id# 128535 La Jolla, California, United States, 92037 University of California, Los Angeles /ID# 127262 Los Angeles, California, United States, 90095 Stanford Univ School of Med /ID# 126495 Stanford, California, United States, 94305-2200 United States, District of Columbia Medstar Georgetown Univ Med Ct /ID# 127261 Washington, District of Columbia, United States, 20007 United States, Georgia Emory University Hospital /ID# 131249 Atlanta, Georgia, United States, 30322 United States, Illinois Northwestern University /ID# 126497 Chicago, Illinois, United States, 60611-2927 United States, Massachusetts Beth Israel Deaconess Med Ctr /ID# 134509 Boston, Massachusetts, United States, 02215-5400 Dana-Farber Cancer Institute /ID# 126496 Boston, Massachusetts, United States, 02215 United States, Minnesota Mayo Clinic - Rochester /ID# 130013 Rochester, Minnesota, United States, 55905-0001 United States, New York Columbia Univ Medical Center /ID# 128536 New York, New York, United States, 10032-3725 New York Presbyterian Hospital - Weill Cornell Medical Center /ID# 129648 New York, New York, United States, 10032-3725 Univ Rochester Med Ctr /ID# 130011 Rochester, New York, United States, 14642 United States, Ohio The Ohio State University - Columbus /ID# 127263 Columbus, Ohio, United States, 43210 United States, Pennsylvania University of Pennsylvania /ID# 126860 Philadelphia, Pennsylvania, United States, 19104-5502 United States, Texas Univ TX, MD Anderson /ID# 126498 Houston, Texas, United States, 77030 United States, Utah University of Utah /ID# 129984 Salt Lake City, Utah, United States, 84112-5500 University of Utah /ID# 130813 Salt Lake City, Utah, United States, 84112-5500 收起 <<

Idelalisib/艾代拉里斯 参考文献

[1]Lannutti BJ, Meadows SA, et al. CAL-101, a p110delta selective phosphatidylinositol-3-kinase inhibitor for the treatment of B-cell malignancies, inhibits PI3K signaling and cellular viability. Blood. 2011 Jan 13;117(2):591-4.

[2]Zhao HF, Wang J, et al. Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development. Mol Cancer. 2017 Jun 7;16(1):100.

[3]Herman SE, Gordon AL, et al. Phosphatidylinositol 3-kinase-δ inhibitor CAL-101 shows promising preclinical activity in chronic lymphocytic leukemia by antagonizing intrinsic and extrinsic cellular survival signals. Blood. 2010 Sep 23;116(12):2078-88.

[4]Cheah CY, Fowler NH, et al. Idelalisib in the management of lymphoma. Blood. 2016 Jul 21;128(3):331-6.

[5]Berndt A, Miller S, et al. The p110 delta structure: mechanisms for selectivity and potency of new PI(3)K inhibitors. Nat Chem Biol. 2010 Feb;6(2):117-24.

[6]Ahmad S, Abu-Eid R, et al. Differential PI3Kδ Signaling in CD4+ T-cell Subsets Enables Selective Targeting of T Regulatory Cells to Enhance Cancer Immunotherapy. Cancer Res. 2017;77(8):1892-1904.

[7]Low PC, Manzanero S, et al. PI3Kδ inhibition reduces TNF secretion and neuroinflammation in a mouse cerebral stroke model. Nat Commun. 2014.

Idelalisib/艾代拉里斯 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

2.41mL

0.48mL

0.24mL

12.04mL

2.41mL

1.20mL

24.07mL

4.81mL

2.41mL

Idelalisib/艾代拉里斯 技术信息

CAS号870281-82-6
分子式C22H18FN7O
分子量 415.42
SMILES Code O=C1N(C2=CC=CC=C2)C([C@@H](NC3=C4N=CNC4=NC=N3)CC)=NC5=C1C(F)=CC=C5
MDL No. MFCD19443647
别名 CAL-101; GS-1101; GS-1101, Idelalisib.
运输蓝冰
InChI Key IFSDAJWBUCMOAH-HNNXBMFYSA-N
Pubchem ID 11625818
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, inert atmosphere, 2-8°C

溶解方案

DMSO: 60 mg/mL(144.43 mM),注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO

请根据您的动物给药指南选择适当的溶解方案。
以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂:
——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
方案 一
方案 二
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