Eganelisib | IPI-549 | PI3Kγ Inhibitor | AmBeed-信号通路专用抑制剂

Eganelisib {[allProObj[0].p_purity_real_show]}

货号：A175847 同义名： IPI-549

Eganelisib 是一种选择性的磷脂酰肌醇-3-激酶（PI3K）-γ抑制剂，IC50为16 nM。

Eganelisib 化学结构
CAS号：1693758-51-8

Eganelisib 3D分子结构
CAS号：1693758-51-8

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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			Sirtuin,PKC,Src	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						✔		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。

Eganelisib 生物活性

靶点

p110γ

PI3Kγ, IC50:16 nM

描述

PI3Ks are divided into three classes (I, II, and III) based on substrate speciﬁcity, sequence homology, and types of regulatory subunits. Class I PI3Ks are further divided into Class IA and Class IB. Class IB of PI3Ks containing the only member, PI3Kγ, is activated primarily by G-protein coupled receptors. The PI3Kγ isoform is mainly expressed in immune cells. Preclinical studies suggest that PI3Kγ inhibition in tumor-associated myeloid cells may be eﬀective to prevent tumor growth. IPI-549 is a potent inhibitor of PI3Kγ (IC50 = 16 nM, measured by Promega ADP-Glo Max assay kit) with >100-fold selectivity over other lipid and protein kinases. IPI-549 shows excellent PI3Kγ potency (IC50 = 1.2 nM) and selectivity against other Class I PI3K isoforms (>146-fold) measured by cellular phospho-AKT inhibition assays in SKOV-3, 786-O, RAW 264.7, and RAJI cells. Also, IPI-549 inhibited PI3Kγ-dependent BMDM migration in a dose-dependent manner in vitro. 0.1 - 3 mg/kg oral treatment of IPI-549 signiﬁcantly reduced neutrophil migration in a dose-dependent manner while a significant inhibition of PI3Kγ can be observed in the mouse air pouch model. IPI-549 is currently in Phase 1 clinical evaluation of advanced solid tumors^[1].

Eganelisib 细胞实验

Cell Line DC2.4 cells MDSCs M2 macrophages derived from RAW264.7 cells MiPS-LLCcm MiPS-PK8cm MiPS-T47Dcm Human PBMCs CT26 cells Murine splenocytes Adipose-derived stem cells (ADSCs) SW620/Ad300 cells LLC-PK-MDR1 cells Bone marrow-derived macrophages (BMDMs)	Concentration	Treated Time	Description	References
DC2.4 cells	100 µL	3 hours	To observe the uptake of PMA-NeoV by DCs	J Immunother Cancer. 2022 Feb;10(2):e003564.
MDSCs	2 µg/mL	12 hours	To evaluate the inhibitory effect of LIC on MDSCs, results showed that LIC significantly reduced Arg-1 and ROS levels and promoted MDSCs apoptosis	Adv Sci (Weinh). 2021 Jul;8(14):e2100712.
M2 macrophages derived from RAW264.7 cells	5 µM	14 days	The combination of IPI-549 and PTX completely inhibited 3D MTC growth, while the combination of IPI-549 with other chemotherapeutic agents (doxorubicin and gemcitabine) did not show improvement compared to single drug treatment.	Sci Transl Med. 2022 May 4;14(643):eabl3649.
MiPS-LLCcm	14.6 µM	48 hours	Inhibited proliferation, self-renewal, migration, and invasion of miPS-LLCcm cells and induced apoptosis	Sci Rep. 2022 Jan 10;12(1):347.
MiPS-PK8cm	18.1 µM	48 hours	Inhibited proliferation, self-renewal, migration, and invasion of miPS-PK8cm cells and induced apoptosis	Sci Rep. 2022 Jan 10;12(1):347.
MiPS-T47Dcm	16.38 µM	48 hours	Inhibited proliferation, self-renewal, migration, and invasion of miPS-T47Dcm cells and induced apoptosis	Sci Rep. 2022 Jan 10;12(1):347.
Human PBMCs	1 µM	6 hours	To investigate the effect of Eganelisib on T cell activation, results showed that Eganelisib reduced the frequency of CD69+ cells.	Hemasphere. 2023 Feb 22;7(3):e840.
CT26 cells	0.8 µM	6 hours	To evaluate the cytotoxicity of LIC on CT26 cells, results showed that LIC significantly induced apoptosis under laser irradiation	Adv Sci (Weinh). 2021 Jul;8(14):e2100712.
Murine splenocytes	1 µM	72 hours	To investigate the effect of Eganelisib on T cell proliferation, results showed that Eganelisib reduced the proliferation rate of T cells.	Hemasphere. 2023 Feb 22;7(3):e840.
Adipose-derived stem cells (ADSCs)	100 nM	72 hours	To evaluate the effect of IPI-549 on the differentiation of adipose-derived stem cells, results showed that IPI-549 significantly reduced lipid accumulation and normalized it to the control level.	Front Immunol. 2022 Dec 20;13:1004609.
SW620/Ad300 cells	5 µM and 10 µM	72 hours	IPI-549 significantly sensitized SW620/Ad300 cells to ABCB1 substrates, increased the intracellular concentration of paclitaxel, and inhibited the efflux of paclitaxel.	Cancer Lett. 2019 Feb 1;442:91-103.
LLC-PK-MDR1 cells	2.5 µM and 5 µM	72 hours	IPI-549 significantly reduced the resistance of LLC-PK-MDR1 cells to ABCB1 substrate drugs.	Cancer Lett. 2019 Feb 1;442:91-103.
Bone marrow-derived macrophages (BMDMs)	5 µM		Enhanced M2 to M1 macrophage polarization, shown by increased M1 markers (TNF-α and IL-12) and decreased M2 markers (IL-10 and TGF-β).	Sci Transl Med. 2022 May 4;14(643):eabl3649.

Cell Line

Concentration

Treated Time

Description

References

DC2.4 cells

100 µL

3 hours

To observe the uptake of PMA-NeoV by DCs

J Immunother Cancer. 2022 Feb;10(2):e003564.

MDSCs

2 µg/mL

12 hours

To evaluate the inhibitory effect of LIC on MDSCs, results showed that LIC significantly reduced Arg-1 and ROS levels and promoted MDSCs apoptosis

Adv Sci (Weinh). 2021 Jul;8(14):e2100712.

M2 macrophages derived from RAW264.7 cells

5 µM

14 days

The combination of IPI-549 and PTX completely inhibited 3D MTC growth, while the combination of IPI-549 with other chemotherapeutic agents (doxorubicin and gemcitabine) did not show improvement compared to single drug treatment.

Sci Transl Med. 2022 May 4;14(643):eabl3649.

MiPS-LLCcm

14.6 µM

48 hours

Inhibited proliferation, self-renewal, migration, and invasion of miPS-LLCcm cells and induced apoptosis

Sci Rep. 2022 Jan 10;12(1):347.

MiPS-PK8cm

18.1 µM

48 hours

Inhibited proliferation, self-renewal, migration, and invasion of miPS-PK8cm cells and induced apoptosis

Sci Rep. 2022 Jan 10;12(1):347.

MiPS-T47Dcm

16.38 µM

48 hours

Inhibited proliferation, self-renewal, migration, and invasion of miPS-T47Dcm cells and induced apoptosis

Sci Rep. 2022 Jan 10;12(1):347.

Human PBMCs

1 µM

6 hours

To investigate the effect of Eganelisib on T cell activation, results showed that Eganelisib reduced the frequency of CD69+ cells.

Hemasphere. 2023 Feb 22;7(3):e840.

CT26 cells

0.8 µM

6 hours

To evaluate the cytotoxicity of LIC on CT26 cells, results showed that LIC significantly induced apoptosis under laser irradiation

Adv Sci (Weinh). 2021 Jul;8(14):e2100712.

Murine splenocytes

1 µM

72 hours

To investigate the effect of Eganelisib on T cell proliferation, results showed that Eganelisib reduced the proliferation rate of T cells.

Hemasphere. 2023 Feb 22;7(3):e840.

Adipose-derived stem cells (ADSCs)

100 nM

72 hours

To evaluate the effect of IPI-549 on the differentiation of adipose-derived stem cells, results showed that IPI-549 significantly reduced lipid accumulation and normalized it to the control level.

Front Immunol. 2022 Dec 20;13:1004609.

SW620/Ad300 cells

5 µM and 10 µM

72 hours

IPI-549 significantly sensitized SW620/Ad300 cells to ABCB1 substrates, increased the intracellular concentration of paclitaxel, and inhibited the efflux of paclitaxel.

Cancer Lett. 2019 Feb 1;442:91-103.

LLC-PK-MDR1 cells

2.5 µM and 5 µM

72 hours

IPI-549 significantly reduced the resistance of LLC-PK-MDR1 cells to ABCB1 substrate drugs.

Cancer Lett. 2019 Feb 1;442:91-103.

Bone marrow-derived macrophages (BMDMs)

5 µM

Enhanced M2 to M1 macrophage polarization, shown by increased M1 markers (TNF-α and IL-12) and decreased M2 markers (IL-10 and TGF-β).

Sci Transl Med. 2022 May 4;14(643):eabl3649.

Eganelisib 动物实验

Species C57BL/6J and Balb/c mice C57BL/6 mice C57BL/6J mice Athymic mice BALB/c mice BALB/c Nude mice Mice	Animal Model 4T1 breast cancer model, B16-GMCSF melanoma model Pancreatic cancer and melanoma models MC38 tumor model SW620/Ad300 xenograft tumor model CT26 tumor model MiPS-LLCcm xenograft model MMTV-PyMT transgenic mice and 4T1 orthotopic breast cancer model	Administration	Dosage	Frequency	Description	References
C57BL/6J and Balb/c mice	4T1 breast cancer model, B16-GMCSF melanoma model	Oral gavage	15 mg/kg	Once daily for 14 days	To evaluate the inhibitory effect of IPI-549 on tumor growth and metastasis, the results showed that IPI-549 significantly inhibited tumor growth and reduced lung metastasis.	Nature. 2016 Nov 17;539(7629):443-447
C57BL/6 mice	Pancreatic cancer and melanoma models	Intravenous injection	15 mg/kg	Every three days, continuous treatment	IPI-549 NP significantly decreased tumor growth and prolonged host survival in both models, reshaping the suppressive tumor microenvironment by decreasing both suppressive myeloid and plasma cells in the tumor.	J Control Release. 2019 Sep 10;309:173-180
C57BL/6J mice	MC38 tumor model	Oral	225 µg	Daily for 2 weeks	To evaluate the tumor suppression effect of IPI-549 combined with PMA-NeoV on MC38 tumors	J Immunother Cancer. 2022 Feb;10(2):e003564.
Athymic mice	SW620/Ad300 xenograft tumor model	Intraperitoneal injection	3 mg/kg IPI-549 and 15 mg/kg paclitaxel	Every 3 days for a total of 4 doses	IPI-549 enhanced the anti-tumor effects of paclitaxel on ABCB1-overexpressing MDR SW620/Ad300 tumors.	Cancer Lett. 2019 Feb 1;442:91-103.
BALB/c mice	CT26 tumor model	Tail vein injection	3.0 mg/kg	Once every other day for 15 days	To evaluate the antitumor effect of LIC in vivo, results showed that LIC significantly inhibited tumor growth and enhanced immune response	Adv Sci (Weinh). 2021 Jul;8(14):e2100712.
BALB/c Nude mice	MiPS-LLCcm xenograft model	Intraperitoneal injection	5 mg/kg	Every other day for 12 days	Eganelisib significantly inhibited tumor growth, reduced tumor volume and weight, and induced tumor cell apoptosis	Sci Rep. 2022 Jan 10;12(1):347.
Mice	MMTV-PyMT transgenic mice and 4T1 orthotopic breast cancer model	Intravenous injection (IV)	PTX (10 mg/kg) and IPI-549 (5 mg/kg)	Once every 3 days for 5 doses	The combination of Nano-PI with α-PD1 achieved long-term tumor remission, eliminated lung metastasis, and significantly improved mouse survival in MMTV-PyMT transgenic mice.	Sci Transl Med. 2022 May 4;14(643):eabl3649.

Species

C57BL/6J and Balb/c mice C57BL/6 mice C57BL/6J mice Athymic mice BALB/c mice BALB/c Nude mice Mice

Animal Model

4T1 breast cancer model, B16-GMCSF melanoma model Pancreatic cancer and melanoma models MC38 tumor model SW620/Ad300 xenograft tumor model CT26 tumor model MiPS-LLCcm xenograft model MMTV-PyMT transgenic mice and 4T1 orthotopic breast cancer model

Administration

Dosage

Frequency

Description

References

C57BL/6J and Balb/c mice

4T1 breast cancer model, B16-GMCSF melanoma model

Oral gavage

15 mg/kg

Once daily for 14 days

To evaluate the inhibitory effect of IPI-549 on tumor growth and metastasis, the results showed that IPI-549 significantly inhibited tumor growth and reduced lung metastasis.

Nature. 2016 Nov 17;539(7629):443-447

C57BL/6 mice

Pancreatic cancer and melanoma models

Intravenous injection

15 mg/kg

Every three days, continuous treatment

IPI-549 NP significantly decreased tumor growth and prolonged host survival in both models, reshaping the suppressive tumor microenvironment by decreasing both suppressive myeloid and plasma cells in the tumor.

J Control Release. 2019 Sep 10;309:173-180

C57BL/6J mice

MC38 tumor model

Oral

225 µg

Daily for 2 weeks

To evaluate the tumor suppression effect of IPI-549 combined with PMA-NeoV on MC38 tumors

J Immunother Cancer. 2022 Feb;10(2):e003564.

Athymic mice

SW620/Ad300 xenograft tumor model

Intraperitoneal injection

3 mg/kg IPI-549 and 15 mg/kg paclitaxel

Every 3 days for a total of 4 doses

IPI-549 enhanced the anti-tumor effects of paclitaxel on ABCB1-overexpressing MDR SW620/Ad300 tumors.

Cancer Lett. 2019 Feb 1;442:91-103.

BALB/c mice

CT26 tumor model

Tail vein injection

3.0 mg/kg

Once every other day for 15 days

To evaluate the antitumor effect of LIC in vivo, results showed that LIC significantly inhibited tumor growth and enhanced immune response

Adv Sci (Weinh). 2021 Jul;8(14):e2100712.

BALB/c Nude mice

MiPS-LLCcm xenograft model

Intraperitoneal injection

5 mg/kg

Every other day for 12 days

Eganelisib significantly inhibited tumor growth, reduced tumor volume and weight, and induced tumor cell apoptosis

Sci Rep. 2022 Jan 10;12(1):347.

Mice

MMTV-PyMT transgenic mice and 4T1 orthotopic breast cancer model

Intravenous injection (IV)

PTX (10 mg/kg) and IPI-549 (5 mg/kg)

Once every 3 days for 5 doses

The combination of Nano-PI with α-PD1 achieved long-term tumor remission, eliminated lung metastasis, and significantly improved mouse survival in MMTV-PyMT transgenic mice.

Sci Transl Med. 2022 May 4;14(643):eabl3649.

Eganelisib 动物研究

Dose

Mice: 15 mg/kg^[2] (p.o.), 3 mg/kg^[3] (i.p.)

Administration

p.o, i.p.

Pharmacokinetics

Animal	Mice^[1]	Rats^[1]	Dogs^[1]	Monkeys^[1]
Dose	1 mg/kg	1 mg/kg	0.5 mg/kg	0.5 mg/kg
Administration	i.v.	i.v.	i.v.	i.v.
T_1/2	3.2 h	4.4 h	6.7 h	4.3 h
Vss	0.8 L/kg	1.2 L/kg	1.3 L/kg	1.3 L/kg
CL	3.6 ml/min/kg	4.4 ml/min/kg	2.8 ml/min/kg	4.3 ml/min/kg
F	0.88	0.57	0.65	0.31

Eganelisib 参考文献

Eganelisib 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

1.89mL

0.38mL

0.19mL

9.46mL

1.89mL

0.95mL

18.92mL

3.78mL

1.89mL

Eganelisib 技术信息

CAS号	1693758-51-8
分子式	C₃₀H₂₄N₈O₂
分子量	528.56
SMILES Code	O=C(C1=C2N=CC=CN2N=C1N)N[C@H](C3=CC4=C(C(N3C5=CC=CC=C5)=O)C(C#CC6=CN(C)N=C6)=CC=C4)C
MDL No.	MFCD30533720

别名	IPI-549
运输	蓝冰
InChI Key	XUMALORDVCFWKV-IBGZPJMESA-N
Pubchem ID	91933883

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: 25 mg/mL(47.3 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

Eganelisib {[allProObj[0].p_purity_real_show]}

Eganelisib 纯度/质量文件产品仅供科研

全球学术期刊中引用的产品

Eganelisib 质控信息

Eganelisib 生物活性

Eganelisib 细胞实验

Eganelisib 动物实验

Eganelisib 动物研究

Eganelisib 参考文献

Eganelisib 实验方案

Eganelisib 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

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

Eganelisib {[allProObj[0].p_purity_real_show]}

Eganelisib 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

Eganelisib 质控信息

Eganelisib 生物活性

Eganelisib 细胞实验

Eganelisib 动物实验

Eganelisib 动物研究

Eganelisib 参考文献

Eganelisib 实验方案

Eganelisib 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

请登录您的专属账户

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

Eganelisib 纯度/质量文件产品仅供科研