HS-173 | PI3K Inhibitor | AmBeed-信号通路专用抑制剂

HS-173 {[allProObj[0].p_purity_real_show]}

货号：A336342

HS-173是一种强效的 PI3Kα 抑制剂，IC50 为 0.8 nM。

HS-173 化学结构
CAS号：1276110-06-5

HS-173 3D分子结构
CAS号：1276110-06-5

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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			PKC,Src,Sirtuin	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						✔		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。

HS-173 生物活性

靶点

p110α

PI3Kα , IC50:0.8 nM

描述

HS-173, at concentrations ranging from 0.1 to 10 μM, diminishes cell viability in a manner that is both concentration and time-dependent. It effectively curbs the growth of colonies in pancreatic cancer cells as the dosage increases. Moreover, HS-173 blocks cell migration and invasion triggered by TGF-β in pancreatic cancer cells and prevents TGF-β-induced epithelial-mesenchymal transition (EMT)^[1]. In experiments with two hepatic stellate cell lines, HS-173 application leads to a reduction in cell viability, influenced by the dosage and duration of treatment. It prompts a halt in the cell cycle at the G2/M phase. The compound elevates levels of cleaved caspase-3 and reduces those of Bcl-2 in HSC-T6 cells. Furthermore, HS-173 curtails the expression of pro-fibrotic mediators and modulators of extracellular matrix (ECM) degradation in hepatic stellate cells (HSCs)^[2]. The co-administration of Sorafenib and HS-173 acts synergistically to halt cell proliferation in pancreatic cancer cell lines, affecting crucial enzymes within the RAF/MAPK and PI3K/AKT signaling pathways^[3].

体内研究

Administered intraperitoneally at 10 mg/kg, HS-173 significantly upregulates TUNEL and cleaved caspase-3 expression while downregulating PCNA expression in tumor tissues. It also diminishes the levels of phosphorylated AKT and Smad2 in these tissues. Doses of 10 and 30 mg/kg of HS-173 markedly reduce metastatic spread to the lungs and liver^[1].

At doses of 10 and 20 mg/kg, HS-173 tackles ECM accumulation and the PI3K/Akt pathway in a mouse model of liver fibrosis induced by CCl4. It notably lowers the levels of phosphorylated Akt and p-P70S6K, alongside reducing collagen I and vimentin expression in the liver fibrosis model^[2].

体外研究

In experiments with two hepatic stellate cell lines, HS-173 application leads to a reduction in cell viability, influenced by the dosage and duration of treatment. It prompts a halt in the cell cycle at the G2/M phase. The compound elevates levels of cleaved caspase-3 and reduces those of Bcl-2 in HSC-T6 cells. Furthermore, HS-173 curtails the expression of pro-fibrotic mediators and modulators of extracellular matrix (ECM) degradation in hepatic stellate cells (HSCs)^[2].

The co-administration of Sorafenib and HS-173 acts synergistically to halt cell proliferation in pancreatic cancer cell lines, affecting crucial enzymes within the RAF/MAPK and PI3K/AKT signaling pathways^[3].

HS-173 细胞实验

Cell Line MG-63 cells CT26 cells KB-3-1 KB-V1 S1 S1-MI-80 MG-63 cells U2OS cells CAL 27 cells FaDu cells CT26 cells	Concentration	Treated Time	Description	References
MG-63 cells	1 nM	1 hour	To investigate the effect of HS-173 on Wnt5a/ROR2-mediated cell migration, the results showed that HS-173 significantly inhibited Wnt5a/ROR2-mediated cell migration.	Cancer Cell Int. 2017 Nov 29;17:112.
CT26 cells	0.01 µM to 50 µM	24 hours	To evaluate the cytotoxicity of PARP and PI3K inhibitor combinations, results showed that the N-H combination significantly enhanced cytotoxicity after radiation.	Mater Today Bio. 2020 Oct 22;8:100082.
KB-3-1	2 µM	24 hours	HS-173 significantly induced G2/M cell cycle arrest	Cells. 2023 Mar 30;12(7):1056.
KB-V1	2 µM	24 hours	G2/M arrest induced by HS-173 was significantly reduced	Cells. 2023 Mar 30;12(7):1056.
S1	2 µM	24 hours	HS-173 significantly induced G2/M cell cycle arrest	Cells. 2023 Mar 30;12(7):1056.
S1-MI-80	2 µM	24 hours	G2/M arrest induced by HS-173 was significantly reduced	Cells. 2023 Mar 30;12(7):1056.
MG-63 cells	1 nM	30 minutes	Wnt5a-induced activation of RhoA was mostly blocked by pretreatment of HS-173 in MG-63 cells	Cancer Cell Int. 2017 Feb 14;17:27.
U2OS cells	1 nM	30 minutes	Wnt5a-induced activation of RhoA was mostly blocked by pretreatment of HS-173 in U2OS cells	Cancer Cell Int. 2017 Feb 14;17:27.
CAL 27 cells	0.125 µM	48 hours	HS-173 showed anti-proliferative effects and induced apoptosis in CAL 27 cells.	Int J Mol Sci. 2023 Jun 21;24(13):10448.
FaDu cells	0.8 µM	48 hours	HS-173 showed anti-proliferative effects and induced apoptosis in FaDu cells.	Int J Mol Sci. 2023 Jun 21;24(13):10448.
CT26 cells	0.4 µM	6 hours	To evaluate the ability of N-H to induce immunogenic cell death, results showed that N-H significantly induced CRT expression.	Mater Today Bio. 2020 Oct 22;8:100082.

Cell Line

Concentration

Treated Time

Description

References

MG-63 cells

1 nM

1 hour

To investigate the effect of HS-173 on Wnt5a/ROR2-mediated cell migration, the results showed that HS-173 significantly inhibited Wnt5a/ROR2-mediated cell migration.

Cancer Cell Int. 2017 Nov 29;17:112.

CT26 cells

0.01 µM to 50 µM

24 hours

To evaluate the cytotoxicity of PARP and PI3K inhibitor combinations, results showed that the N-H combination significantly enhanced cytotoxicity after radiation.

Mater Today Bio. 2020 Oct 22;8:100082.

KB-3-1

2 µM

24 hours

HS-173 significantly induced G2/M cell cycle arrest

Cells. 2023 Mar 30;12(7):1056.

KB-V1

2 µM

24 hours

G2/M arrest induced by HS-173 was significantly reduced

Cells. 2023 Mar 30;12(7):1056.

2 µM

24 hours

HS-173 significantly induced G2/M cell cycle arrest

Cells. 2023 Mar 30;12(7):1056.

S1-MI-80

2 µM

24 hours

G2/M arrest induced by HS-173 was significantly reduced

Cells. 2023 Mar 30;12(7):1056.

MG-63 cells

1 nM

30 minutes

Wnt5a-induced activation of RhoA was mostly blocked by pretreatment of HS-173 in MG-63 cells

Cancer Cell Int. 2017 Feb 14;17:27.

U2OS cells

1 nM

30 minutes

Wnt5a-induced activation of RhoA was mostly blocked by pretreatment of HS-173 in U2OS cells

Cancer Cell Int. 2017 Feb 14;17:27.

CAL 27 cells

0.125 µM

48 hours

HS-173 showed anti-proliferative effects and induced apoptosis in CAL 27 cells.

Int J Mol Sci. 2023 Jun 21;24(13):10448.

FaDu cells

0.8 µM

48 hours

HS-173 showed anti-proliferative effects and induced apoptosis in FaDu cells.

Int J Mol Sci. 2023 Jun 21;24(13):10448.

CT26 cells

0.4 µM

6 hours

To evaluate the ability of N-H to induce immunogenic cell death, results showed that N-H significantly induced CRT expression.

Mater Today Bio. 2020 Oct 22;8:100082.

HS-173 动物实验

Species BALB/c mice	Animal Model CT26 colorectal cancer model	Administration	Dosage	Frequency	Description	References
BALB/c mice	CT26 colorectal cancer model	Tail vein injection	3.57 mg/kg HS-173, 3.69 mg/kg niraparib	Every 2 days, for a total of 3 doses	To evaluate the antitumor efficacy of N-H POx in combination with radiotherapy and immunotherapy, results showed that N-H POx significantly enhanced tumor control and increased tumor infiltrating lymphocytes.	Mater Today Bio. 2020 Oct 22;8:100082.

Species

BALB/c mice

Animal Model

CT26 colorectal cancer model

Administration

Dosage

Frequency

Description

References

BALB/c mice

CT26 colorectal cancer model

Tail vein injection

3.57 mg/kg HS-173, 3.69 mg/kg niraparib

Every 2 days, for a total of 3 doses

To evaluate the antitumor efficacy of N-H POx in combination with radiotherapy and immunotherapy, results showed that N-H POx significantly enhanced tumor control and increased tumor infiltrating lymphocytes.

Mater Today Bio. 2020 Oct 22;8:100082.

HS-173 参考文献

HS-173 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.37mL

0.47mL

0.24mL

11.84mL

2.37mL

1.18mL

23.67mL

4.73mL

2.37mL

HS-173 技术信息

CAS号	1276110-06-5
分子式	C₂₁H₁₈N₄O₄S
分子量	422.46
SMILES Code	O=C(C1=CN=C2C=CC(C3=CC(NS(=O)(C4=CC=CC=C4)=O)=CN=C3)=CN21)OCC
MDL No.	MFCD28023584

别名
运输	蓝冰
InChI Key	SEKOTFCHZNXZMM-UHFFFAOYSA-N
Pubchem ID	52936849

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: 50 mg/mL(118.36 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

细胞研究

细胞系	浓度	检测类型	检测时间	活性说明	数据源

MCF7 cells	Cytotoxicity assay	48 h	Cytotoxicity against human MCF7 cells after 48 hrs by MTT assay, IC50=7.8 μM	21388141
SK-BR-3 cells	Cytotoxicity assay	48 h	Cytotoxicity against human SK-BR-3 cells after 48 hrs by MTT assay, IC50=1.5 μM	21388141
T47D cells	Cytotoxicity assay	48 h	Cytotoxicity against human T47D cells after 48 hrs by MTT assay, IC50=0.6 μM	21388141

HS-173 {[allProObj[0].p_purity_real_show]}

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HS-173 {[allProObj[0].p_purity_real_show]}

HS-173 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

HS-173 质控信息

HS-173 生物活性

HS-173 细胞实验

HS-173 动物实验

HS-173 参考文献

HS-173 实验方案

HS-173 技术信息

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