Voxtalisib | XL765 | PI3K Inhibitor | AmBeed-信号通路专用抑制剂

Voxtalisib {[allProObj[0].p_purity_real_show]}

货号：A393898 同义名： XL765; SAR245409

Voxtalisib是一种强效且高度选择性的 I 类 PI3K 抑制剂，IC50 值分别为 39/110/9/43 nM 对 PI3Kα/β/γ/δ，同时有效抑制 mTOR (IC50 为 160-910 nM)。

Voxtalisib 化学结构
CAS号：934493-76-2

Voxtalisib 3D分子结构
CAS号：934493-76-2

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mTOR 亚型比较

PI3K 亚型比较

产品名称	mTOR ↓ ↑	mTORC1 ↓ ↑	mTORC2 ↓ ↑	其他靶点	纯度
AZD-8055	++++ mTOR (full length), IC50: 0.8 nM mTOR (truncated), IC50: 0.13 nM				99%+
Gedatolisib	++++ mTOR, IC50: 1.6 nM				99%
GSK1059615	++ mTOR, IC50: 12 nM				98%
Vistusertib	+++ mTOR, IC50: 2.8 nM				99%+
Torin 1	+++ mTOR, IC50: 4.32 nM	+++ mTORC1, IC50: 2 nM	++ mTORC2, IC50: 10 nM	DNA-PK	99%+
Dactolisib	+++ mTOR (p70S6K), IC50: 6 nM				98+%
PI-103	+ mTOR, IC50: 30 nM				99%+
WAY-600	++ mTOR, IC50: 9 nM				99%
Voxtalisib	+ mTOR, IC50: 157 nM				99%+
PF-04691502	++ mTOR, Ki: 16 nM				98+%
Onatasertib	++ mTOR, IC50: 16 nM			DNA-PK	99%+
Chrysophanol	✔			EGFR	98%
Samotolisib	✔			DNA-PK	99%+
Torkinib	+++ mTOR, IC50: 8 nM			DNA-PK,PDGFR	99%+
Everolimus					99%+
WYE-354	+++ mTOR, IC50: 5 nM				98%
Tacrolimus	✔				98%
PP121	++ mTOR, IC50: 13 nM			VEGFR,PDGFR	99%+
Torin 2	++++ mTOR, IC50: 0.25 nM			DNA-PK	99%+
Rapamycin	++++ mTOR, IC50: ~0.1 nM				98%
GDC-0349	+++ mTOR, Ki: 3.8 nM				98%
XL388	++ mTOR, IC50: 9.9 nM	+++ mTORC1, IC50: 8 nM	+ mTORC2, IC50: 166 nM		99%+
WYE-687	+++ mTOR, IC50: 7 nM				98%
Apitolisib	+ mTOR, Ki app: 17 nM				98%+
WYE-132	++++ mTOR, IC50: 0.19 nM				99%+
Sapanisertib	++++ mTOR, Ki: 1.4 nM				99%+
BGT226 maleate	✔				99%+
ETP-46464	++++ mTOR, IC50: 0.6 nM			DNA-PK	98%
PI3K-IN-1	+ mTOR, IC50: 157 nM				98+%
Zotarolimus	+++ FKBP-12, IC50: 2.8 nM				98%
OSI-027	+++ mTOR, IC50: 4 nM	+ mTORC1, IC50: 22 nM	+ mTORC2, IC50: 65 nM		99%+
Ridaforolimus	++++ mTOR, IC50: 0.2 nM				99%+
Temsirolimus	+ mTOR, IC50: 1.76 μM				95%
CZ415	++ mTOR, pIC50: 8.07				99%+
SF2523	+ mTOR, IC50: 280 nM			DNA-PK	99%+
KU-0063794		++ mTORC1, IC50: ~10 nM	++ mTORC2, IC50: ~10 nM		99%+
Omipalisib		++++ mTORC1, Ki: 0.18 nM	++++ mTORC2, Ki: 0.3 nM		99%+
Palomid 529		✔			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。

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。

Voxtalisib 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

Activation of the PI3K (phosphoinositide 3-kinase) pathway is a frequent occurrence in human tumors and is thought to promote growth, survival, and resistance to diverse therapies. Voxtalisib (XL765) is a potent and highly selective pan inhibitor of class I PI3Ks (α, β, γ, and δ) with activity against mTOR. In cellular assays, XL765 inhibits the formation of PIP3 in the membrane, and inhibits phosphorylation of AKT, p70S6K, and S6 phosphorylation in multiple tumor cell lines with different genetic alterations affecting the PI3K pathway. XL765 displayed potent inhibitory activity against class I PI3K isoforms p110α, p110β, p110δ, and p120γ, with IC₅₀ values of 39, 110, 43, and 9 nM, respectively, IC₅₀ values of 160 and 910 nM for mTORC1 and mTORC2, respectively. In a vitro study, XL765 inhibits colony growth with an IC₅₀ value of 270 nM in PC-3 cells and 230 nM in MCF7 cells. Oral administration of XL765 (10, 30, 100, or 300 mg/kg) caused a dose-dependent decrease of phosphorylation of AKT, p70S6K, and S6 in the tumors on melanoma xenograft mice, reaching a maximum of 84% inhibition of S6 phosphorylation at 30 mg/kg at 4h^[3].

Voxtalisib 细胞实验

Cell Line U87IDHmut cells MDA-MB-231 MCF-7 Chronic lymphocytic leukemia cells SUM149 and MDA-MB-231 NHAIDHmut cells GBM 39 GBM GS-2 GBM 12 GBM 8 SUM149 TNBC cells MDA-MB-231 ST88 MPNST642 STS26T MPNST724 S462	Concentration	Treated Time	Description	References
U87IDHmut cells	12 µM	24 hours	To evaluate the effect of XL765 on U87IDHmut cell proliferation, showing a 61.0 ± 10.6% reduction in cell number.	Sci Rep. 2019 Jul 19;9(1):10521.
MDA-MB-231	IC50 75.2 µM	24 hours	Investigate the effect of XL765 on circRNA and linRNA expression, showing upregulation of circRNA and downregulation of linRNA	Noncoding RNA. 2023 May 19;9(3):32.
MCF-7	IC50 91.4 µM	24 hours	Investigate the effect of XL765 on circRNA and linRNA expression, showing upregulation of circRNA and downregulation of linRNA	Noncoding RNA. 2023 May 19;9(3):32.
Chronic lymphocytic leukemia cells	0.86 µM (IC50)	48 hours	Therapeutic effect on chronic lymphocytic leukemia through apoptotic caspase-dependent mechanisms and effectively inhibits T-cell-mediated cytokine production	Front Pharmacol. 2022 Jun 14;13:914733.
SUM149 and MDA-MB-231	0.5 µM	6 hours	To assess the effect of combination treatment on TNBC cell migration and invasion capabilities	J Cancer. 2015 Oct 28;6(12):1306-19.
NHAIDHmut cells	32 µM	72 hours	To evaluate the effect of XL765 on NHAIDHmut cell proliferation, showing a 55.7 ± 16% reduction in cell number.	Sci Rep. 2019 Jul 19;9(1):10521.
GBM 39	5.0 µM	72 hours	Evaluate the cytotoxicity of XL765 on GBM 39 cells, showing a concentration-dependent decrease in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM GS-2	7.7 µM	72 hours	Evaluate the cytotoxicity of XL765 on GBM GS-2 cells, showing a concentration-dependent decrease in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM 12	3.7 µM	72 hours	Evaluate the cytotoxicity of XL765 on GBM 12 cells, showing a concentration-dependent decrease in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
GBM 8	5.7 µM	72 hours	Evaluate the cytotoxicity of XL765 on GBM 8 cells, showing a concentration-dependent decrease in cell viability	Neuro Oncol. 2011 Apr;13(4):384-92.
SUM149 TNBC cells	0.005-20 µM	72 hours	Evaluate the synergistic effect of Voxtalisib with birinapant, results showed no significant synergistic effect observed in SUM149 cells	Mol Cancer Ther. 2021 Feb;20(2):296-306.
MDA-MB-231	40 nM	72 hours	To evaluate the synergistic inhibitory effect of PI3K inhibitor SAR245409 combined with MEK inhibitor AS703026 on TNBC cell proliferation	J Cancer. 2015 Oct 28;6(12):1306-19.
ST88	0.25-20 µM	96 hours	XL765 significantly inhibited MPNST cell growth with an 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 an 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 an 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 an 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 an IC50 of 0.81 μM	Mol Cancer Ther. 2012 Aug;11(8):1758-69.

Cell Line

Concentration

Treated Time

Description

References

U87IDHmut cells

12 µM

24 hours

To evaluate the effect of XL765 on U87IDHmut cell proliferation, showing a 61.0 ± 10.6% reduction in cell number.

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

MDA-MB-231

IC50 75.2 µM

24 hours

Investigate the effect of XL765 on circRNA and linRNA expression, showing upregulation of circRNA and downregulation of linRNA

Noncoding RNA. 2023 May 19;9(3):32.

MCF-7

IC50 91.4 µM

24 hours

Investigate the effect of XL765 on circRNA and linRNA expression, showing upregulation of circRNA and downregulation of linRNA

Noncoding RNA. 2023 May 19;9(3):32.

Chronic lymphocytic leukemia cells

0.86 µM (IC50)

48 hours

Therapeutic effect on chronic lymphocytic leukemia through apoptotic caspase-dependent mechanisms and effectively inhibits T-cell-mediated cytokine production

Front Pharmacol. 2022 Jun 14;13:914733.

SUM149 and MDA-MB-231

0.5 µM

6 hours

To assess the effect of combination treatment on TNBC cell migration and invasion capabilities

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

NHAIDHmut cells

32 µM

72 hours

To evaluate the effect of XL765 on NHAIDHmut cell proliferation, showing a 55.7 ± 16% reduction in cell number.

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

GBM 39

5.0 µM

72 hours

Evaluate the cytotoxicity of XL765 on GBM 39 cells, showing a concentration-dependent decrease in cell viability

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

GBM GS-2

7.7 µM

72 hours

Evaluate the cytotoxicity of XL765 on GBM GS-2 cells, showing a concentration-dependent decrease in cell viability

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

GBM 12

3.7 µM

72 hours

Evaluate the cytotoxicity of XL765 on GBM 12 cells, showing a concentration-dependent decrease in cell viability

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

GBM 8

5.7 µM

72 hours

Evaluate the cytotoxicity of XL765 on GBM 8 cells, showing a concentration-dependent decrease in cell viability

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

SUM149 TNBC cells

0.005-20 µM

72 hours

Evaluate the synergistic effect of Voxtalisib with birinapant, results showed no significant synergistic effect observed in SUM149 cells

Mol Cancer Ther. 2021 Feb;20(2):296-306.

MDA-MB-231

40 nM

72 hours

To evaluate the synergistic inhibitory effect of PI3K inhibitor SAR245409 combined with MEK inhibitor AS703026 on TNBC cell proliferation

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

ST88

0.25-20 µM

96 hours

XL765 significantly inhibited MPNST cell growth with an 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 an 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 an 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 an 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 an IC50 of 0.81 μM

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

Voxtalisib 动物实验

Species Nude mice Mice SCID mice Nude mice Mice Nude mice	Animal Model U87IDHmut intracranial tumor model Gastrointestinal stromal tumor (GIST) model MPNST724 and STS26T xenograft models GS-2 and U87-MG GBM orthotopic models Aldh5a1−/− mouse model Intracranial xenograft GBM 39 model	Administration	Dosage	Frequency	Description	References
Nude mice	U87IDHmut intracranial tumor model	Oral	30 mg/kg	Twice daily, continuous treatment	To evaluate the effect of XL765 on U87IDHmut intracranial tumor model, showing that XL765 treatment significantly prolonged animal survival.	Sci Rep. 2019 Jul 19;9(1):10521.
Mice	Gastrointestinal stromal tumor (GIST) model	Oral gavage	30 mg/kg (6-hour treatment), 20 mg/kg (7-day treatment)	Single dose for 6-hour treatment or twice daily for 7-day treatment	To evaluate the effect of Voxtalisib on GIST tumor proliferation. Results showed that 6-hour treatment inhibited PI3K signaling (pAKT, pS6, and p4EBP1) but increased MAPK phosphorylation. Seven days of treatment reduced tumor cell proliferation by 70%.	Proc Natl Acad Sci U S A. 2017 Oct 3;114(40):E8448-E8457
SCID mice	MPNST724 and STS26T xenograft models	Oral	30 mg/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.
Nude mice	GS-2 and U87-MG GBM orthotopic models	Oral	30mg/kg voxtalisib twice daily	Twice daily, continuous treatment	To monitor the effect of voxtalisib alone or in combination with TMZ, finding a significantly lower lactate-to-pyruvate ratio post-treatment, associated with enhanced survival	Mol Cancer Ther. 2016 May;15(5):1113-22
Mice	Aldh5a1−/− mouse model	Intraperitoneal injection	5 mg/kg/day and 10 mg/kg/day	Once daily until death	To evaluate the effects of mTOR inhibitors on lifespan and body weight in aldh5a1?/? mice. Results showed that Tor2, XL-765, and tat-Bec1 significantly extended lifespan and improved body weight.	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, for 2 weeks	Evaluate the inhibitory effect of XL765 on GBM 39 tumor growth in vivo, showing a 13-fold reduction in median tumor bioluminescence and improvement in median survival compared to control	Neuro Oncol. 2011 Apr;13(4):384-92.

Species

Nude mice Mice SCID mice Nude mice Mice Nude mice

Animal Model

U87IDHmut intracranial tumor model Gastrointestinal stromal tumor (GIST) model MPNST724 and STS26T xenograft models GS-2 and U87-MG GBM orthotopic models Aldh5a1−/− mouse model Intracranial xenograft GBM 39 model

Administration

Dosage

Frequency

Description

References

Nude mice

U87IDHmut intracranial tumor model

Oral

30 mg/kg

Twice daily, continuous treatment

To evaluate the effect of XL765 on U87IDHmut intracranial tumor model, showing that XL765 treatment significantly prolonged animal survival.

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

Mice

Gastrointestinal stromal tumor (GIST) model

Oral gavage

30 mg/kg (6-hour treatment), 20 mg/kg (7-day treatment)

Single dose for 6-hour treatment or twice daily for 7-day treatment

To evaluate the effect of Voxtalisib on GIST tumor proliferation. Results showed that 6-hour treatment inhibited PI3K signaling (pAKT, pS6, and p4EBP1) but increased MAPK phosphorylation. Seven days of treatment reduced tumor cell proliferation by 70%.

Proc Natl Acad Sci U S A. 2017 Oct 3;114(40):E8448-E8457

SCID mice

MPNST724 and STS26T xenograft models

Oral

30 mg/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.

Nude mice

GS-2 and U87-MG GBM orthotopic models

Oral

30mg/kg voxtalisib twice daily

Twice daily, continuous treatment

To monitor the effect of voxtalisib alone or in combination with TMZ, finding a significantly lower lactate-to-pyruvate ratio post-treatment, associated with enhanced survival

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

Mice

Aldh5a1−/− mouse model

Intraperitoneal injection

5 mg/kg/day and 10 mg/kg/day

Once daily until death

To evaluate the effects of mTOR inhibitors on lifespan and body weight in aldh5a1?/? mice. Results showed that Tor2, XL-765, and tat-Bec1 significantly extended lifespan and improved body weight.

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, for 2 weeks

Evaluate the inhibitory effect of XL765 on GBM 39 tumor growth in vivo, showing a 13-fold reduction in median tumor bioluminescence and improvement in median survival compared to control

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

Voxtalisib 参考文献

Voxtalisib 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

3.70mL

0.74mL

0.37mL

18.50mL

3.70mL

1.85mL

37.00mL

7.40mL

3.70mL

Voxtalisib 技术信息

CAS号	934493-76-2
分子式	C₁₃H₁₄N₆O
分子量	270.29
SMILES Code	CCN1C2=NC(N)=NC(C)=C2C=C(C3=NNC=C3)C1=O
MDL No.	MFCD20276656

别名	XL765; SAR245409
运输	蓝冰
InChI Key	RGHYDLZMTYDBDT-UHFFFAOYSA-N
Pubchem ID	16123056

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: 9 mg/mL(33.3 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, IC50:9 nM
p110β	PI3Kβ, IC50:113 nM
p110α	PI3Kα, IC50:39 nM
p110δ	PI3Kδ, IC50:43 nM
mTOR	mTOR, IC50:157 nM

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Voxtalisib 技术信息

最近浏览的产品

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