PI3K-IN-1 | XL147 analog 2 | PI3K Inhibitor | AmBeed-信号通路专用抑制剂

PI3K-IN-1 {[allProObj[0].p_purity_real_show]}

货号：A781923 同义名： XL147 analog 2; SAR245409

PI3K-IN-1是一种双重抑制剂，能够同时抑制 mTOR 和 PI3K，主要作用于 p110γ，IC50 为 9 nM，同时抑制 DNA-PK 和 mTOR。

PI3K-IN-1 化学结构
CAS号：1349796-36-6

PI3K-IN-1 3D分子结构
CAS号：1349796-36-6

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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				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		DNA-PK,MLCK	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。

PI3K-IN-1 生物活性

靶点

p110γ

PI3Kγ, IC50:9 nM
p110β

PI3Kβ, IC50:113 nM
p110α

PI3Kα, IC50:39 nM
p110δ

PI3Kδ, IC50:43 nM
mTOR

mTOR, IC50:157 nM

描述

XL765 analogue is a dual inhibitor of mTOR/PI3K, mostly for p110γ with IC50 of 9 nM, and also inhibits DNA-PK and mTOR.

PI3K-IN-1 细胞实验

Cell Line Rat nucleus pulposus-derived mesenchymal stem cells U87IDHmut cells SUM149 and MDA-MB-231 GBM 39 GBM GS-2 GBM 12 GBM 8 GBM 6 NHAIDHmut cells MDA-MB-231 ST88-14 MPNST642 STS26T MPNST724 S462	Concentration	Treated Time	Description	References
Rat nucleus pulposus-derived mesenchymal stem cells	25 µM	2 hours	Inhibited the PI3K/Akt pathway, weakening the protective effect of melatonin against H2O2-induced oxidative stress injury	J Orthop Translat. 2023 Dec 2;43:66-84.
U87IDHmut cells	12 µM	24 hours	To assess the effect of XL765 on cell proliferation, resulting in a 61.0 ± 10.6% reduction in cell number	Sci Rep. 2019 Jul 19;9(1):10521.
SUM149 and MDA-MB-231	0.5 µM	6 hours	Evaluate the inhibitory effect of XL765 combined with AS703026 on TNBC cell migration and invasion ability. Results showed that the combination significantly inhibited cell migration and invasion (p <0.001).	J Cancer. 2015 Oct 28;6(12):1306-19.
GBM 39	5.0 µM	72 hours	XL765 resulted in concentration-dependent decreases in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM GS-2	7.7 µM	72 hours	XL765 resulted in concentration-dependent decreases in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM 12	3.7 µM	72 hours	XL765 resulted in concentration-dependent decreases in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM 8	5.7 µM	72 hours	XL765 resulted in concentration-dependent decreases in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM 6	7.5 µM	72 hours	XL765 resulted in concentration-dependent decreases in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
NHAIDHmut cells	32 µM	72 hours	To assess the effect of XL765 on cell proliferation, resulting in a 55.7 ± 16% reduction in cell number	Sci Rep. 2019 Jul 19;9(1):10521.
MDA-MB-231	40 nM	72 hours	Evaluate the synergistic inhibitory effect of XL765 combined with AS703026 on TNBC cell proliferation. Results showed that the combination significantly inhibited cell proliferation (P < 0.001).	J Cancer. 2015 Oct 28;6(12):1306-19.
ST88-14	0.25-20 µM	96 hours	XL765 significantly inhibited MPNST cell growth with IC50 of 2.49 μM	Mol Cancer Ther. 2012 Aug;11(8):1758-69.
MPNST642	0.25-20 µM	96 hours	XL765 significantly inhibited MPNST cell growth with IC50 of 1.93 μM	Mol Cancer Ther. 2012 Aug;11(8):1758-69.
STS26T	0.25-20 µM	96 hours	XL765 significantly inhibited MPNST cell growth with IC50 of 1.75 μM	Mol Cancer Ther. 2012 Aug;11(8):1758-69.
MPNST724	0.25-20 µM	96 hours	XL765 significantly inhibited MPNST cell growth with IC50 of 0.86 μM	Mol Cancer Ther. 2012 Aug;11(8):1758-69.
S462	0.25-20 µM	96 hours	XL765 significantly inhibited MPNST cell growth with IC50 of 0.81 μM	Mol Cancer Ther. 2012 Aug;11(8):1758-69.

Cell Line

Concentration

Treated Time

Description

References

Rat nucleus pulposus-derived mesenchymal stem cells

25 µM

2 hours

Inhibited the PI3K/Akt pathway, weakening the protective effect of melatonin against H2O2-induced oxidative stress injury

J Orthop Translat. 2023 Dec 2;43:66-84.

U87IDHmut cells

12 µM

24 hours

To assess the effect of XL765 on cell proliferation, resulting in a 61.0 ± 10.6% reduction in cell number

Sci Rep. 2019 Jul 19;9(1):10521.

SUM149 and MDA-MB-231

0.5 µM

6 hours

Evaluate the inhibitory effect of XL765 combined with AS703026 on TNBC cell migration and invasion ability. Results showed that the combination significantly inhibited cell migration and invasion (p <0.001).

J Cancer. 2015 Oct 28;6(12):1306-19.

GBM 39

5.0 µM

72 hours

XL765 resulted in concentration-dependent decreases in cell viability

Neuro Oncol. 2011 Apr;13(4):384-92.

GBM GS-2

7.7 µM

72 hours

XL765 resulted in concentration-dependent decreases in cell viability

Neuro Oncol. 2011 Apr;13(4):384-92.

GBM 12

3.7 µM

72 hours

XL765 resulted in concentration-dependent decreases in cell viability

Neuro Oncol. 2011 Apr;13(4):384-92.

GBM 8

5.7 µM

72 hours

XL765 resulted in concentration-dependent decreases in cell viability

Neuro Oncol. 2011 Apr;13(4):384-92.

GBM 6

7.5 µM

72 hours

XL765 resulted in concentration-dependent decreases in cell viability

Neuro Oncol. 2011 Apr;13(4):384-92.

NHAIDHmut cells

32 µM

72 hours

To assess the effect of XL765 on cell proliferation, resulting in a 55.7 ± 16% reduction in cell number

Sci Rep. 2019 Jul 19;9(1):10521.

MDA-MB-231

40 nM

72 hours

Evaluate the synergistic inhibitory effect of XL765 combined with AS703026 on TNBC cell proliferation. Results showed that the combination significantly inhibited cell proliferation (P < 0.001).

J Cancer. 2015 Oct 28;6(12):1306-19.

ST88-14

0.25-20 µM

96 hours

XL765 significantly inhibited MPNST cell growth with IC50 of 2.49 μM

Mol Cancer Ther. 2012 Aug;11(8):1758-69.

MPNST642

0.25-20 µM

96 hours

XL765 significantly inhibited MPNST cell growth with IC50 of 1.93 μM

Mol Cancer Ther. 2012 Aug;11(8):1758-69.

STS26T

0.25-20 µM

96 hours

XL765 significantly inhibited MPNST cell growth with IC50 of 1.75 μM

Mol Cancer Ther. 2012 Aug;11(8):1758-69.

MPNST724

0.25-20 µM

96 hours

XL765 significantly inhibited MPNST cell growth with IC50 of 0.86 μM

Mol Cancer Ther. 2012 Aug;11(8):1758-69.

S462

0.25-20 µM

96 hours

XL765 significantly inhibited MPNST cell growth with IC50 of 0.81 μM

Mol Cancer Ther. 2012 Aug;11(8):1758-69.

PI3K-IN-1 动物实验

Species Athymic nu/nu mice Nude mice SCID mice Mice Nude mice	Animal Model U87IDHmut orthotopic tumor model GS-2 and U87-MG glioblastoma models MPNST724 and STS26T xenograft models Aldehyde dehydrogenase 5a1-deficient mouse model Intracranial xenograft GBM 39 model	Administration	Dosage	Frequency	Description	References
Athymic nu/nu mice	U87IDHmut orthotopic tumor model	Oral	30 mg/kg	Twice daily until the end of the experiment	To evaluate the effect of XL765 on tumor growth and animal survival, showing that XL765 significantly prolonged animal survival but did not significantly affect tumor volume	Sci Rep. 2019 Jul 19;9(1):10521.
Nude mice	GS-2 and U87-MG glioblastoma models	Oral	30mg/kg voxtalisib twice daily, 5mg/kg TMZ daily	Daily administration until tumor was no longer detectable or animals had to be sacrificed	To evaluate the effects of XL765 alone or in combination with TMZ on glioblastoma models, showing a significantly lower lactate-to-pyruvate ratio in treated groups, which was associated with enhanced animal survival.	Mol Cancer Ther. 2016 May;15(5):1113-22
SCID mice	MPNST724 and STS26T xenograft models	Oral	30mg/kg/bid	Twice daily, continuous treatment	XL765 significantly inhibited local and metastatic growth of MPNST xenografts	Mol Cancer Ther. 2012 Aug;11(8):1758-69.
Mice	Aldehyde dehydrogenase 5a1-deficient mouse model	Intraperitoneal injection	5 mg/kg/day	Once daily, up to 50 days	XL-765 significantly extended the lifespan of aldh5a1?/? mice and induced weight gain	J Inherit Metab Dis. 2016 Nov;39(6):877-886
Nude mice	Intracranial xenograft GBM 39 model	Oral gavage	50 mg/kg	Twice daily (6 hours apart) on days 21–25, 28–32, 49–53, and 56–60	XL765 shows activity as monotherapy and in combination with conventional therapeutics in a range of genetically diverse GBM xenografts. In vivo, XL765 administered by oral gavage resulted in greater than 12-fold reduction in median tumor bioluminescence compared with control (Mann–Whitney test p=0.001) and improvement in median survival (logrank p=0.05). TMZ alone showed a 30-fold decrease in median bioluminescence, but the combination XL765 + TMZ yielded a 140-fold reduction in median bioluminescence (Mann-Whitney test p=0.05) with a trend toward improvement in median survival (logrank p=0.09) compared with TMZ alone.	Neuro Oncol. 2011 Apr;13(4):384-92.

Species

Athymic nu/nu mice Nude mice SCID mice Mice Nude mice

Animal Model

U87IDHmut orthotopic tumor model GS-2 and U87-MG glioblastoma models MPNST724 and STS26T xenograft models Aldehyde dehydrogenase 5a1-deficient mouse model Intracranial xenograft GBM 39 model

Administration

Dosage

Frequency

Description

References

Athymic nu/nu mice

U87IDHmut orthotopic tumor model

Oral

30 mg/kg

Twice daily until the end of the experiment

To evaluate the effect of XL765 on tumor growth and animal survival, showing that XL765 significantly prolonged animal survival but did not significantly affect tumor volume

Sci Rep. 2019 Jul 19;9(1):10521.

Nude mice

GS-2 and U87-MG glioblastoma models

Oral

30mg/kg voxtalisib twice daily, 5mg/kg TMZ daily

Daily administration until tumor was no longer detectable or animals had to be sacrificed

To evaluate the effects of XL765 alone or in combination with TMZ on glioblastoma models, showing a significantly lower lactate-to-pyruvate ratio in treated groups, which was associated with enhanced animal survival.

Mol Cancer Ther. 2016 May;15(5):1113-22

SCID mice

MPNST724 and STS26T xenograft models

Oral

30mg/kg/bid

Twice daily, continuous treatment

XL765 significantly inhibited local and metastatic growth of MPNST xenografts

Mol Cancer Ther. 2012 Aug;11(8):1758-69.

Mice

Aldehyde dehydrogenase 5a1-deficient mouse model

Intraperitoneal injection

5 mg/kg/day

Once daily, up to 50 days

XL-765 significantly extended the lifespan of aldh5a1?/? mice and induced weight gain

J Inherit Metab Dis. 2016 Nov;39(6):877-886

Nude mice

Intracranial xenograft GBM 39 model

Oral gavage

50 mg/kg

Twice daily (6 hours apart) on days 21–25, 28–32, 49–53, and 56–60

XL765 shows activity as monotherapy and in combination with conventional therapeutics in a range of genetically diverse GBM xenografts. In vivo, XL765 administered by oral gavage resulted in greater than 12-fold reduction in median tumor bioluminescence compared with control (Mann–Whitney test p=0.001) and improvement in median survival (logrank p=0.05). TMZ alone showed a 30-fold decrease in median bioluminescence, but the combination XL765 + TMZ yielded a 140-fold reduction in median bioluminescence (Mann-Whitney test p=0.05) with a trend toward improvement in median survival (logrank p=0.09) compared with TMZ alone.

Neuro Oncol. 2011 Apr;13(4):384-92.

PI3K-IN-1 参考文献

PI3K-IN-1 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

1.67mL

0.33mL

0.17mL

8.34mL

1.67mL

0.83mL

16.68mL

3.34mL

1.67mL

PI3K-IN-1 技术信息

CAS号	1349796-36-6
分子式	C₃₁H₂₉N₅O₆S
分子量	599.66
SMILES Code	O=C(NC1=CC=C(S(=O)(NC2=NC3=CC=CC=C3N=C2NC4=CC(OC)=CC(OC)=C4)=O)C=C1)C5=CC=C(C)C(OC)=C5
MDL No.	MFCD18252649

别名	XL147 analog 2; SAR245409; SAR245409-Analog; XL765-Analog; Voxtalisib-Analog; Voxtalisib Analogue; XL-147 derivative 1
运输	蓝冰
InChI Key	HJSSPYJVWLTYHG-UHFFFAOYSA-N
Pubchem ID	49867926

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry,2-8°C

溶解方案

细胞实验：

DMSO: 25 mg/mL(41.69 mM)，配合低频超声，并水浴加热至45℃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

靶点

靶点	数值

p110γ	PI3Kγ, IC50:9 nM
p110β	PI3Kβ, IC50:113 nM
p110α	PI3Kα, IC50:39 nM
p110δ	PI3Kδ, IC50:43 nM
mTOR	mTOR, IC50:157 nM

PI3K-IN-1 {[allProObj[0].p_purity_real_show]}

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PI3K-IN-1 质控信息

PI3K-IN-1 生物活性

PI3K-IN-1 细胞实验

PI3K-IN-1 动物实验

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靶点	p110γ PI3Kγ, IC50:9 nM p110β PI3Kβ, IC50:113 nM p110α PI3Kα, IC50:39 nM p110δ PI3Kδ, IC50:43 nM mTOR mTOR, IC50:157 nM
描述	XL765 analogue is a dual inhibitor of mTOR/PI3K, mostly for p110γ with IC50 of 9 nM, and also inhibits DNA-PK and mTOR.

PI3K-IN-1 {[allProObj[0].p_purity_real_show]}

PI3K-IN-1 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

PI3K-IN-1 质控信息

PI3K-IN-1 生物活性

PI3K-IN-1 细胞实验

PI3K-IN-1 动物实验

PI3K-IN-1 参考文献

PI3K-IN-1 实验方案

PI3K-IN-1 技术信息

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摩尔计算器

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总药量计算器

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细胞研究

临床研究

确认信息

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PI3K-IN-1 纯度/质量文件产品仅供科研