AZD8186 | PI3K | AmBeed-信号通路专用抑制剂

AZD8186 {[allProObj[0].p_purity_real_show]}

货号：A160272

AZD8186是一种同源特异性的PI3K抑制剂，能强效抑制PI3Kβ（IC50 = 4 nM）和PI3Kδ（IC50 = 12 nM），对PI3Kα（IC50 = 35 nM）和PI3Kγ（IC50 = 675 nM）具有选择性。

AZD8186 化学结构
CAS号：1627494-13-6

AZD8186 3D分子结构
CAS号：1627494-13-6

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PI3K 亚型比较

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				DNA-PK,mTOR	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			DNA-PK,mTOR	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			DNA-PK,mTOR	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			DNA-PK,mTOR	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						✔		PTEN,Akt	99%+
NU 7026						+ PI3K, IC50: 13 μM		DNA-PK	98+%
Deguelin						✔		Akt	99%+
Ailanthone						✔		CDK,Akt,ATM/ATR	98%
Resibufogenin						✔		ROS	98%
KU-57788						+ PI3K, IC50: 5 μM		DNA-PK,mTOR	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。

AZD8186 生物活性

靶点

p110β

PI3Kβ, IC50:4 nM
p110α

PI3Kα, IC50:35 nM
p110δ

PI3Kδ, IC50:12 nM

描述

Several studies have highlighted the dependency of PTEN deficiency to PI3Kβ activity. For example, conditional knockout of PIK3CB, the gene coding for the p110β subunit, can block the formation of prostate tumours in mouse models, which shows the important role of PI3Kβ in the occurrence of prostate tumour driven by PTEN loss/mutant^[1]. AZD8186 is a potent and selective inhibitor of PI3Kβ/δ with IC50 of 4 nM and 12 nM (measured by using a Kinase-Glo Plus Assay Kit), respectively, less potent to PI3Kα (IC50=35 nM)^[2]. Treatment of 3 nM of AZD8186 can inhibit 50% level of PI3Kβ-dependent activation of pAKT-Ser473 in PTEN-null, MDA-MB-468, cell line, as well as 17 nM of AZD8186 can inhibit IgM-stimulated pAKT-Ser473, which is activated through PI3Kδ, in JEKO cells. These indicate AZD8186 selectively inhibits PI3Kβ- andδ-mediated signaling through AKT in vitro. In the study of growth inhibition by AZD8186, it was found that AZD8186 is effective in breast and prostate lines, but show more reliable on loss of PTEN in prostate lines. AZD8186 is effective to combination therapy in prostate cancer preclinical models. 10 and 30 mg/kg AZD8186 with 15 mg/kg docetaxel showed regressions in PC3 tumor model^[3].

AZD8186 细胞实验

Cell Line K422 HT OCI-Ly10 TMD8 Riva MDA-MB-468 HCC70 EVSA-T ZR-75-1 LNCaP KYSE70 cells MKN45 and MKN28 gastric cancer cells BT-549 A2780 A2780CP70 HAC-2 Daoy cells DU145-DR PC3-DR BT-474 HNSCC cells	Concentration	Treated Time	Description	References
K422	0.5 µM	24 hours	Induced G0/G1 cell cycle arrest	Leukemia. 2023 Jan;37(1):178-189.
HT	0.5 µM	24 hours	Induced G0/G1 cell cycle arrest	Leukemia. 2023 Jan;37(1):178-189.
OCI-Ly10	0.5 µM	48 hours	Induced apoptosis	Leukemia. 2023 Jan;37(1):178-189.
TMD8	0.5 µM	48 hours	Induced apoptosis	Leukemia. 2023 Jan;37(1):178-189.
Riva	0.5 µM	48 hours	Induced apoptosis	Leukemia. 2023 Jan;37(1):178-189.
MDA-MB-468	0.5 µM	1, 3, 6, and 24 hours	To assess the effect of PI3K β inhibition on metabolic pathway activities in a PTEN null breast cancer cell line, the results showed that AZD8186 significantly altered 286 isotope-enriched features, of which 19 features could be attributed to known targeted pathways.	Front Mol Biosci. 2022 Oct 14;9:1004602.
HCC70	100 nM	14-21 days	To screen for genes conferring resistance to the PI3Kβ inhibitor AZD8186	Oncogene. 2022 Nov;41(46):5046-5060.
EVSA-T	250 nM	14-21 days	To screen for genes conferring resistance to the PI3Kβ inhibitor AZD8186	Oncogene. 2022 Nov;41(46):5046-5060.
ZR-75-1	50 nM	14-21 days	To screen for genes conferring resistance to the PI3Kβ inhibitor AZD8186	Oncogene. 2022 Nov;41(46):5046-5060.
LNCaP	25 nM	2 hours	AZD8186 at 25 nM significantly inhibited Akt phosphorylation in LNCaP cells	Cancer Cell. 2015 Jan 12;27(1):109-22.
KYSE70 cells	3 μg/ml, 30 μg/ml	24 hours	To evaluate cell apoptosis and cell cycle distribution, results showed AZD8186 induced cell apoptosis and G1 phase arrest.	Nanomedicine. 2018 Oct;14(7):2103-2114.
MKN45 and MKN28 gastric cancer cells	0, 10, 50, 100, 200, 500 µM	24 hours and 48 hours	To evaluate the inhibitory effect of AZD8186 on gastric cancer cells, the results showed that AZD8186 exhibited a dose-dependent inhibitory effect on MKN45 and MKN28 cells after 24 and 48 hours.	Front Pharmacol. 2024 Jun 19;15:1355269.
BT-549	250 nM	30 minutes	AZD8186 at 250 nM significantly inhibited Akt phosphorylation in BT-549 cells within 30 minutes	Cancer Cell. 2015 Jan 12;27(1):109-22.
A2780	4.08 µM (IC50)	48 hours	To evaluate the inhibitory effect of AZD8186 on A2780 cells, the results showed that PI3KCA-mutated cells were more sensitive to AZD8186.	Front Pharmacol. 2020 Mar 3;11:206.
A2780CP70	7.27 µM (IC50)	48 hours	To evaluate the inhibitory effect of AZD8186 on A2780CP70 cells, the results showed that PI3KCA-mutated cells were more sensitive to AZD8186.	Front Pharmacol. 2020 Mar 3;11:206.
HAC-2	6.66 µM (IC50)	48 hours	To evaluate the inhibitory effect of AZD8186 on HAC-2 cells, the results showed that PI3KCA-mutated cells were more sensitive to AZD8186.	Front Pharmacol. 2020 Mar 3;11:206.
Daoy cells	1 µM	6 hours	Inhibition of PI3K/AKT/mTOR signaling pathway, detection of SOX9 protein degradation	EMBO J. 2016 Oct 17;35(20):2192-2212.
DU145-DR	5 µM	72 hours	AZD8186 alone strongly suppressed AKT and GSK3 β phosphorylation and, to a lesser degree, S6 phosphorylation.	Front Pharmacol. 2024 Jan 22;15:1331648.
PC3-DR	5 µM	72 hours	AZD8186 alone strongly suppressed AKT and GSK3 β phosphorylation and, to a lesser degree, S6 phosphorylation.	Front Pharmacol. 2024 Jan 22;15:1331648.
BT-474	250 nM		AZD8186 at 250 nM had no significant effect on Akt/mTOR signaling in BT-474 cells	Cancer Cell. 2015 Jan 12;27(1):109-22.
HNSCC cells	1.5 µM		AZD8186 enhances radio- and radiochemosensitivity in the majority of HNSCC cell models, independent of PIK3CA mutation status	Biomed Pharmacother. 2024 Feb;171:116217.

Cell Line

Concentration

Treated Time

Description

References

K422

0.5 µM

24 hours

Induced G0/G1 cell cycle arrest

Leukemia. 2023 Jan;37(1):178-189.

0.5 µM

24 hours

Induced G0/G1 cell cycle arrest

Leukemia. 2023 Jan;37(1):178-189.

OCI-Ly10

0.5 µM

48 hours

Induced apoptosis

Leukemia. 2023 Jan;37(1):178-189.

TMD8

0.5 µM

48 hours

Induced apoptosis

Leukemia. 2023 Jan;37(1):178-189.

Riva

0.5 µM

48 hours

Induced apoptosis

Leukemia. 2023 Jan;37(1):178-189.

MDA-MB-468

0.5 µM

1, 3, 6, and 24 hours

To assess the effect of PI3K β inhibition on metabolic pathway activities in a PTEN null breast cancer cell line, the results showed that AZD8186 significantly altered 286 isotope-enriched features, of which 19 features could be attributed to known targeted pathways.

Front Mol Biosci. 2022 Oct 14;9:1004602.

HCC70

100 nM

14-21 days

To screen for genes conferring resistance to the PI3Kβ inhibitor AZD8186

Oncogene. 2022 Nov;41(46):5046-5060.

EVSA-T

250 nM

14-21 days

To screen for genes conferring resistance to the PI3Kβ inhibitor AZD8186

Oncogene. 2022 Nov;41(46):5046-5060.

ZR-75-1

50 nM

14-21 days

To screen for genes conferring resistance to the PI3Kβ inhibitor AZD8186

Oncogene. 2022 Nov;41(46):5046-5060.

LNCaP

25 nM

2 hours

AZD8186 at 25 nM significantly inhibited Akt phosphorylation in LNCaP cells

Cancer Cell. 2015 Jan 12;27(1):109-22.

KYSE70 cells

3 μg/ml, 30 μg/ml

24 hours

To evaluate cell apoptosis and cell cycle distribution, results showed AZD8186 induced cell apoptosis and G1 phase arrest.

Nanomedicine. 2018 Oct;14(7):2103-2114.

MKN45 and MKN28 gastric cancer cells

0, 10, 50, 100, 200, 500 µM

24 hours and 48 hours

To evaluate the inhibitory effect of AZD8186 on gastric cancer cells, the results showed that AZD8186 exhibited a dose-dependent inhibitory effect on MKN45 and MKN28 cells after 24 and 48 hours.

Front Pharmacol. 2024 Jun 19;15:1355269.

BT-549

250 nM

30 minutes

AZD8186 at 250 nM significantly inhibited Akt phosphorylation in BT-549 cells within 30 minutes

Cancer Cell. 2015 Jan 12;27(1):109-22.

A2780

4.08 µM (IC50)

48 hours

To evaluate the inhibitory effect of AZD8186 on A2780 cells, the results showed that PI3KCA-mutated cells were more sensitive to AZD8186.

Front Pharmacol. 2020 Mar 3;11:206.

A2780CP70

7.27 µM (IC50)

48 hours

To evaluate the inhibitory effect of AZD8186 on A2780CP70 cells, the results showed that PI3KCA-mutated cells were more sensitive to AZD8186.

Front Pharmacol. 2020 Mar 3;11:206.

HAC-2

6.66 µM (IC50)

48 hours

To evaluate the inhibitory effect of AZD8186 on HAC-2 cells, the results showed that PI3KCA-mutated cells were more sensitive to AZD8186.

Front Pharmacol. 2020 Mar 3;11:206.

Daoy cells

1 µM

6 hours

Inhibition of PI3K/AKT/mTOR signaling pathway, detection of SOX9 protein degradation

EMBO J. 2016 Oct 17;35(20):2192-2212.

DU145-DR

5 µM

72 hours

AZD8186 alone strongly suppressed AKT and GSK3 β phosphorylation and, to a lesser degree, S6 phosphorylation.

Front Pharmacol. 2024 Jan 22;15:1331648.

PC3-DR

5 µM

72 hours

AZD8186 alone strongly suppressed AKT and GSK3 β phosphorylation and, to a lesser degree, S6 phosphorylation.

Front Pharmacol. 2024 Jan 22;15:1331648.

BT-474

250 nM

AZD8186 at 250 nM had no significant effect on Akt/mTOR signaling in BT-474 cells

Cancer Cell. 2015 Jan 12;27(1):109-22.

HNSCC cells

1.5 µM

AZD8186 enhances radio- and radiochemosensitivity in the majority of HNSCC cell models, independent of PIK3CA mutation status

Biomed Pharmacother. 2024 Feb;171:116217.

AZD8186 动物实验

Species Nude mice Nude mice NOD/SCID mice BALB/c (nu/nu) mice Mice Nude-Foxn1nu mice Mice	Animal Model KYSE70 esophageal cancer xenograft model HCC70 and PC3 xenograft models NOD/SCID mice DU145-DR xenograft model OCI-Ly10 and K422 xenograft models HCC70 tumor xenograft model LNCaP xenograft model	Administration	Dosage	Frequency	Description	References
Nude mice	KYSE70 esophageal cancer xenograft model	Tail vein injection	10mg/kg	Every three days for 21 days	To evaluate the anti-tumor efficacy of AZD8186-DCM and DTX-DCM combination therapy, results showed that the combination therapy significantly inhibited tumor growth.	Nanomedicine. 2018 Oct;14(7):2103-2114.
Nude mice	HCC70 and PC3 xenograft models	Oral	25 mg/kg or 50 mg/kg	Single dose or every 12 hours for 1 week	To evaluate the inhibitory effects of AZD8186 on AKT and rpS6 phosphorylation. In the HCC70 xenograft model, AZD8186 suppressed phosphorylation of AKT1, AKT2, and rpS6 for 4 to 7 hours post-single dose, but levels returned to baseline by 24 hours. In the PC3 xenograft model, AZD8186 suppressed phosphorylation of AKT3 at all doses tested.	Mol Cancer Ther. 2021 Apr;20(4):749-760
NOD/SCID mice	NOD/SCID mice	Oral	25 or 50 mg/kg	Twice daily, 5 days on, 2 days off	To evaluate the inhibitory effect of AZD8186 on tumor growth in mice, the results showed that AZD8186 significantly inhibited the growth of ES2 tumors.	Front Pharmacol. 2020 Mar 3;11:206.
BALB/c (nu/nu) mice	DU145-DR xenograft model	Oral	40 mg/kg	Twice daily for 18 days	The combination of AZD8186 with selumetinib significantly reduced tumor growth without showing toxicity.	Front Pharmacol. 2024 Jan 22;15:1331648.
Mice	OCI-Ly10 and K422 xenograft models		50 mg/kg	Daily, for 35 days	Combination of AZD8186 and AZD2014 significantly reduced tumor growth	Leukemia. 2023 Jan;37(1):178-189.
Nude-Foxn1nu mice	HCC70 tumor xenograft model	Oral	66.6 mg/kg	Once daily for 7 days	To evaluate the anti-tumor activity of AZD8186 in combination with AZD5991	Oncogene. 2022 Nov;41(46):5046-5060.
Mice	LNCaP xenograft model	EC50	75 mg/kg	Single dose	AZD8186 at a single dose of 75 mg/kg significantly inhibited Akt signaling in the LNCaP xenograft model, but the signaling rebounded after 8 hours	Cancer Cell. 2015 Jan 12;27(1):109-22.

Species

Nude mice Nude mice NOD/SCID mice BALB/c (nu/nu) mice Mice Nude-Foxn1nu mice Mice

Animal Model

KYSE70 esophageal cancer xenograft model HCC70 and PC3 xenograft models NOD/SCID mice DU145-DR xenograft model OCI-Ly10 and K422 xenograft models HCC70 tumor xenograft model LNCaP xenograft model

Administration

Dosage

Frequency

Description

References

Nude mice

KYSE70 esophageal cancer xenograft model

Tail vein injection

10mg/kg

Every three days for 21 days

To evaluate the anti-tumor efficacy of AZD8186-DCM and DTX-DCM combination therapy, results showed that the combination therapy significantly inhibited tumor growth.

Nanomedicine. 2018 Oct;14(7):2103-2114.

Nude mice

HCC70 and PC3 xenograft models

Oral

25 mg/kg or 50 mg/kg

Single dose or every 12 hours for 1 week

To evaluate the inhibitory effects of AZD8186 on AKT and rpS6 phosphorylation. In the HCC70 xenograft model, AZD8186 suppressed phosphorylation of AKT1, AKT2, and rpS6 for 4 to 7 hours post-single dose, but levels returned to baseline by 24 hours. In the PC3 xenograft model, AZD8186 suppressed phosphorylation of AKT3 at all doses tested.

Mol Cancer Ther. 2021 Apr;20(4):749-760

NOD/SCID mice

Oral

25 or 50 mg/kg

Twice daily, 5 days on, 2 days off

To evaluate the inhibitory effect of AZD8186 on tumor growth in mice, the results showed that AZD8186 significantly inhibited the growth of ES2 tumors.

Front Pharmacol. 2020 Mar 3;11:206.

BALB/c (nu/nu) mice

DU145-DR xenograft model

Oral

40 mg/kg

Twice daily for 18 days

The combination of AZD8186 with selumetinib significantly reduced tumor growth without showing toxicity.

Front Pharmacol. 2024 Jan 22;15:1331648.

Mice

OCI-Ly10 and K422 xenograft models

50 mg/kg

Daily, for 35 days

Combination of AZD8186 and AZD2014 significantly reduced tumor growth

Leukemia. 2023 Jan;37(1):178-189.

Nude-Foxn1nu mice

HCC70 tumor xenograft model

Oral

66.6 mg/kg

Once daily for 7 days

To evaluate the anti-tumor activity of AZD8186 in combination with AZD5991

Oncogene. 2022 Nov;41(46):5046-5060.

Mice

LNCaP xenograft model

EC50

75 mg/kg

Single dose

AZD8186 at a single dose of 75 mg/kg significantly inhibited Akt signaling in the LNCaP xenograft model, but the signaling rebounded after 8 hours

Cancer Cell. 2015 Jan 12;27(1):109-22.

AZD8186 动物研究

Dose

Mice: 25 mg/kg, 50 mg/kg^[3] (s.c.), 60 mg/kg^[2] (p.o.)

Administration

s.c., p.o.

Pharmacokinetics

Animal	Mice	Dogs
Dose	30 μmol/kg
Administration	p.o.	p.o.
CL	77 mL/min/kg	36 mL/min/kg
F	0.18	0.23
AUC	1.2 μM·h
V_d	1.3 L/kg	2.2 L/kg

AZD8186 参考文献

AZD8186 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.19mL

0.44mL

0.22mL

10.93mL

2.19mL

1.09mL

21.86mL

4.37mL

2.19mL

AZD8186 技术信息

CAS号	1627494-13-6
分子式	C₂₄H₂₅F₂N₃O₄
分子量	457.47
SMILES Code	O=C(C1=CC(C(C=C(N2CCOCC2)O3)=O)=C3C([C@H](NC4=CC(F)=CC(F)=C4)C)=C1)N(C)C
MDL No.	MFCD27987908

别名
运输	蓝冰
InChI Key	LMJFJIDLEAWOQJ-CQSZACIVSA-N
Pubchem ID	52913813

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

细胞实验：

DMSO: 35 mg/mL(76.51 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

动物实验：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

方案三

方案四

方案五

方案六

AZD8186 {[allProObj[0].p_purity_real_show]}

AZD8186 纯度/质量文件产品仅供科研

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AZD8186 质控信息

AZD8186 生物活性

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AZD8186 动物实验

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AZD8186 参考文献

AZD8186 实验方案

AZD8186 技术信息

最近浏览的产品

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p110β	PI3Kβ, IC50:4 nM
p110α	PI3Kα, IC50:35 nM
p110δ	PI3Kδ, IC50:12 nM

AZD8186 {[allProObj[0].p_purity_real_show]}

AZD8186 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

AZD8186 质控信息

AZD8186 生物活性

AZD8186 细胞实验

AZD8186 动物实验

AZD8186 动物研究

AZD8186 参考文献

AZD8186 实验方案

AZD8186 技术信息

最近浏览的产品

大规格询价

摩尔计算器

靶点

总药量计算器

工作液计算器

细胞研究

临床研究

确认信息

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AZD8186 纯度/质量文件产品仅供科研