AZD-8835 | PI3K Inhibitor | AmBeed-信号通路专用抑制剂

AZD-8835 {[allProObj[0].p_purity_real_show]}

货号：A279294

AZD8835 是一种有效的选择性PI3Kα和PI3Kδ抑制剂，IC50值分别为6.2 nM和5.7 nM。

AZD-8835 化学结构
CAS号：1620576-64-8

AZD-8835 3D分子结构
CAS号：1620576-64-8

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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。

AZD-8835 生物活性

靶点

p110γ

PI3Kγ, IC50:90 nM
p110β

PI3Kβ, IC50:431 nM
p110α

PI3Kα, IC50:6.2 nM
p110δ

PI3Kδ, IC50:5.7 nM

描述

AZD8835 ia a mixed inhibitor of PI3Kα and PI3Kδ with IC50 of 6.2 nM and 5.7 nM, respectively, also with selectivity against PI3Kβ (IC50=431 nM) and PI3Kγ (IC50=90 nM).

AZD-8835 细胞实验

Cell Line OVCAR-8 HAC-2 A2780CP70 A2780 MCF10A-PI3KαH1047R T47D MCF7 A204 cells SJCRH30 cells RD cells PEO1 T-ALL cell lines BmE cells BmE cells	Concentration	Treated Time	Description	References
OVCAR-8	21.14-53.60 μM	48 hours	AZD8835 inhibited BRCA1/BRCA2 mRNA expression and p-ERK protein expression.	Front Pharmacol. 2020 Mar 3;11:206.
HAC-2	4.64-9.41 μM	48 hours	AZD8835 inhibited Akt phosphorylation and suppressed the expression of Akt downstream effectors 4E-BP1 and p70S6 kinase.	Front Pharmacol. 2020 Mar 3;11:206.
A2780CP70	4.64-9.41 μM	48 hours	AZD8835 inhibited Akt phosphorylation and suppressed the expression of Akt downstream effectors 4E-BP1 and p70S6 kinase.	Front Pharmacol. 2020 Mar 3;11:206.
A2780	4.64-9.41 μM	48 hours	AZD8835 inhibited Akt phosphorylation and suppressed the expression of Akt downstream effectors 4E-BP1 and p70S6 kinase.	Front Pharmacol. 2020 Mar 3;11:206.
MCF10A-PI3KαH1047R	250 nM	24 hours	MAP3K1 knock-down in MCF10A-PI3KαH1047R made cells less sensitive to AZD8835-mediated pathway inhibition, as assessed by pPRAS40 signal.	Oncotarget. 2018 Apr 20;9(30):21444-21458.
T47D	250 nM	24 hours	MAP3K1 knock-down in T47D made cells less sensitive to AZD8835-mediated pathway inhibition, as assessed by pPRAS40 signal.	Oncotarget. 2018 Apr 20;9(30):21444-21458.
MCF7	250 nM	24 hours	MAP3K1 deficiency led to reduced inhibition of the pathway by AZD8835 and AZD5363 with a more pronounced effect on AZD5363 activity, indicated by maintained pP70S6K, pPRAS40 and pS6 ribosomal protein (RP) readouts in CR1.4 and CR2.5 compared with parent cells.	Oncotarget. 2018 Apr 20;9(30):21444-21458.
A204 cells	5 μM	72 hours	Evaluate the effect of AZD8835 on A204 cell viability, results showed AZD8835 reduced cell viability	Molecules. 2022 Apr 24;27(9):2742.
SJCRH30 cells	5 μM	72 hours	Evaluate the effect of AZD8835 on SJCRH30 cell viability, results showed AZD8835 reduced cell viability	Molecules. 2022 Apr 24;27(9):2742.
RD cells	5 μM	72 hours	Evaluate the effect of AZD8835 on RD cell viability, results showed AZD8835 reduced cell viability	Molecules. 2022 Apr 24;27(9):2742.
PEO1	100 nM	24 h and 48 h	Inhibits the PI3K/AKT pathway, reduces cell proliferation and induces cell death	Biomedicines. 2022 Aug 24;10(9):2060.
T-ALL cell lines	0.5 μM		To evaluate the effect of AZD8835 on the proliferation of T-ALL cell lines, showing varying degrees of sensitivity to AZD8835.	Oncotarget. 2016 Apr 19;7(16):22128-39.
BmE cells	10 µM	72 hours	Evaluate the inhibitory effect of AZD8835 on BmNPV, showing accumulated virus DNA of 42%.	Molecules. 2019 Apr 1;24(7):1260.
BmE cells	10 µM	72 hours	Evaluate the cytotoxicity of AZD8835 on BmE cells, showing a cell viability of 83%.	Molecules. 2019 Apr 1;24(7):1260.

Cell Line

Concentration

Treated Time

Description

References

OVCAR-8

21.14-53.60 μM

48 hours

AZD8835 inhibited BRCA1/BRCA2 mRNA expression and p-ERK protein expression.

Front Pharmacol. 2020 Mar 3;11:206.

HAC-2

4.64-9.41 μM

48 hours

AZD8835 inhibited Akt phosphorylation and suppressed the expression of Akt downstream effectors 4E-BP1 and p70S6 kinase.

Front Pharmacol. 2020 Mar 3;11:206.

A2780CP70

4.64-9.41 μM

48 hours

AZD8835 inhibited Akt phosphorylation and suppressed the expression of Akt downstream effectors 4E-BP1 and p70S6 kinase.

Front Pharmacol. 2020 Mar 3;11:206.

A2780

4.64-9.41 μM

48 hours

AZD8835 inhibited Akt phosphorylation and suppressed the expression of Akt downstream effectors 4E-BP1 and p70S6 kinase.

Front Pharmacol. 2020 Mar 3;11:206.

MCF10A-PI3KαH1047R

250 nM

24 hours

MAP3K1 knock-down in MCF10A-PI3KαH1047R made cells less sensitive to AZD8835-mediated pathway inhibition, as assessed by pPRAS40 signal.

Oncotarget. 2018 Apr 20;9(30):21444-21458.

T47D

250 nM

24 hours

MAP3K1 knock-down in T47D made cells less sensitive to AZD8835-mediated pathway inhibition, as assessed by pPRAS40 signal.

Oncotarget. 2018 Apr 20;9(30):21444-21458.

MCF7

250 nM

24 hours

MAP3K1 deficiency led to reduced inhibition of the pathway by AZD8835 and AZD5363 with a more pronounced effect on AZD5363 activity, indicated by maintained pP70S6K, pPRAS40 and pS6 ribosomal protein (RP) readouts in CR1.4 and CR2.5 compared with parent cells.

Oncotarget. 2018 Apr 20;9(30):21444-21458.

A204 cells

5 μM

72 hours

Evaluate the effect of AZD8835 on A204 cell viability, results showed AZD8835 reduced cell viability

Molecules. 2022 Apr 24;27(9):2742.

SJCRH30 cells

5 μM

72 hours

Evaluate the effect of AZD8835 on SJCRH30 cell viability, results showed AZD8835 reduced cell viability

Molecules. 2022 Apr 24;27(9):2742.

RD cells

5 μM

72 hours

Evaluate the effect of AZD8835 on RD cell viability, results showed AZD8835 reduced cell viability

Molecules. 2022 Apr 24;27(9):2742.

PEO1

100 nM

24 h and 48 h

Inhibits the PI3K/AKT pathway, reduces cell proliferation and induces cell death

Biomedicines. 2022 Aug 24;10(9):2060.

T-ALL cell lines

0.5 μM

To evaluate the effect of AZD8835 on the proliferation of T-ALL cell lines, showing varying degrees of sensitivity to AZD8835.

Oncotarget. 2016 Apr 19;7(16):22128-39.

BmE cells

10 µM

72 hours

Evaluate the inhibitory effect of AZD8835 on BmNPV, showing accumulated virus DNA of 42%.

Molecules. 2019 Apr 1;24(7):1260.

BmE cells

10 µM

72 hours

Evaluate the cytotoxicity of AZD8835 on BmE cells, showing a cell viability of 83%.

Molecules. 2019 Apr 1;24(7):1260.

AZD-8835 动物实验

Species NOD/SCID mice Mice Silkworm larvae Nude mice (nu/nu:Alpk)	Animal Model Ovarian cancer xenograft model CT-26, MC-38 and 4T1 tumor models BmNPV infection model BT474C breast xenograft model	Administration	Dosage	Frequency	Description	References
NOD/SCID mice	Ovarian cancer xenograft model	Oral	50 or 100 mg/kg	Once daily, 2 days on: 5 days off for 21 days	AZD8835 significantly inhibited tumor formation.	Front Pharmacol. 2020 Mar 3;11:206.
Mice	CT-26, MC-38 and 4T1 tumor models	Oral	50 mg/kg	2 days on/5 days off for 4 cycles	AZD8835 significantly inhibited tumor growth by suppressing PI3Kα/δ signaling, enhanced CD8+ T-cell activation and memory function, and reduced immunosuppression by T-regs cells.	J Immunother Cancer. 2018 Dec 27;6(1):158
Silkworm larvae	BmNPV infection model	Oral	125 µg/g	Only once	Evaluate the inhibitory effect of AZD8835 on BmNPV in silkworm larvae, showing viral DNA content of 48% and mortality reduced to 12%.	Molecules. 2019 Apr 1;24(7):1260.
Nude mice (nu/nu:Alpk)	BT474C breast xenograft model	Oral gavage	3, 6, 12.5, 25 or 50 mg/kg	Single dose, imaging performed 2 hours post-dose	To evaluate the minimally effective dose of AZD8835, a selective inhibitor of PI3Kα and PI3Kδ, and validate its potential as a pharmacodynamic biomarker using 18F-FDG PET imaging. Results showed that AZD8835 significantly reduced tumor 18F-FDG uptake at doses of 12.5, 25, and 50 mg/kg, with no significant reduction at 3 and 6 mg/kg.	PLoS One. 2017 Aug 14;12(8):e0183048

Species

NOD/SCID mice Mice Silkworm larvae Nude mice (nu/nu:Alpk)

Animal Model

Ovarian cancer xenograft model CT-26, MC-38 and 4T1 tumor models BmNPV infection model BT474C breast xenograft model

Administration

Dosage

Frequency

Description

References

NOD/SCID mice

Ovarian cancer xenograft model

Oral

50 or 100 mg/kg

Once daily, 2 days on: 5 days off for 21 days

AZD8835 significantly inhibited tumor formation.

Front Pharmacol. 2020 Mar 3;11:206.

Mice

CT-26, MC-38 and 4T1 tumor models

Oral

50 mg/kg

2 days on/5 days off for 4 cycles

AZD8835 significantly inhibited tumor growth by suppressing PI3Kα/δ signaling, enhanced CD8+ T-cell activation and memory function, and reduced immunosuppression by T-regs cells.

J Immunother Cancer. 2018 Dec 27;6(1):158

Silkworm larvae

BmNPV infection model

Oral

125 µg/g

Only once

Evaluate the inhibitory effect of AZD8835 on BmNPV in silkworm larvae, showing viral DNA content of 48% and mortality reduced to 12%.

Molecules. 2019 Apr 1;24(7):1260.

Nude mice (nu/nu:Alpk)

BT474C breast xenograft model

Oral gavage

3, 6, 12.5, 25 or 50 mg/kg

Single dose, imaging performed 2 hours post-dose

To evaluate the minimally effective dose of AZD8835, a selective inhibitor of PI3Kα and PI3Kδ, and validate its potential as a pharmacodynamic biomarker using 18F-FDG PET imaging. Results showed that AZD8835 significantly reduced tumor 18F-FDG uptake at doses of 12.5, 25, and 50 mg/kg, with no significant reduction at 3 and 6 mg/kg.

PLoS One. 2017 Aug 14;12(8):e0183048

AZD-8835 参考文献

AZD-8835 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.13mL

0.43mL

0.21mL

10.65mL

2.13mL

1.06mL

21.30mL

4.26mL

2.13mL

AZD-8835 技术信息

CAS号	1620576-64-8
分子式	C₂₂H₃₁N₉O₃
分子量	469.54
SMILES Code	CC(C)(C1=NN=C(O1)C2=NC(C3=NC(C4CCN(CC4)C(CCO)=O)=NN3CC)=CN=C2N)C
MDL No.	MFCD28902194

别名
运输	蓝冰

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, store in freezer, under -20°C

溶解方案

细胞实验：

DMSO: 12 mg/mL(25.56 mM)，配合低频超声助溶，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

靶点

靶点	数值

p110γ	PI3Kγ, IC50:90 nM
p110β	PI3Kβ, IC50:431 nM
p110α	PI3Kα, IC50:6.2 nM
p110δ	PI3Kδ, IC50:5.7 nM

AZD-8835 {[allProObj[0].p_purity_real_show]}

AZD-8835 纯度/质量文件产品仅供科研

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AZD-8835 质控信息

AZD-8835 生物活性

AZD-8835 细胞实验

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靶点	p110γ PI3Kγ, IC50:90 nM p110β PI3Kβ, IC50:431 nM p110α PI3Kα, IC50:6.2 nM p110δ PI3Kδ, IC50:5.7 nM
描述	AZD8835 ia a mixed inhibitor of PI3Kα and PI3Kδ with IC50 of 6.2 nM and 5.7 nM, respectively, also with selectivity against PI3Kβ (IC50=431 nM) and PI3Kγ (IC50=90 nM).

AZD-8835 {[allProObj[0].p_purity_real_show]}

AZD-8835 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

AZD-8835 质控信息

AZD-8835 生物活性

AZD-8835 细胞实验

AZD-8835 动物实验

AZD-8835 参考文献

AZD-8835 实验方案

AZD-8835 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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AZD-8835 纯度/质量文件产品仅供科研