Sophocarpine | 13,14-Dehydromatrine | Autophagy Inducer | AmBeed-信号通路专用抑制剂

Sophocarpine/槐果碱 {[allProObj[0].p_purity_real_show]}

货号：A400441 同义名： 13,14-Dehydromatrine

Sophocarpine是一种来源于植物苦参的天然产物，具有抗肿瘤活性，能够通过抑制胃癌细胞生长，诱导自噬及细胞凋亡，且对多种癌细胞有效，包括肝细胞癌和前列腺癌。

HazMat Fee +

There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.

Type	HazMat fee for 500 gram (Estimated)
Excepted Quantity	USD 0.00
Limited Quantity	USD 15-60
Inaccessible (Haz class 6.1), Domestic	USD 80+
Inaccessible (Haz class 6.1), International	USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic	USD 100+
Accessible (Haz class 3, 4, 5 or 8), International	USD 200+

Sophocarpine/槐果碱化学结构
CAS号：6483-15-4

Sophocarpine/槐果碱 3D分子结构
CAS号：6483-15-4

规格	价格	会员价	库存	数量
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PI3K 亚型比较

钾通道亚型比较

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,Sirtuin,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		MLCK,DNA-PK	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,CDK,ATM/ATR	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。

产品名称	Potassium Channel ↓ ↑	纯度
Tolbutamide	✔	98%
Glimepiride	++++ SUR2B, IC50: 7.3 nM SUR1, IC50: 5.4 nM	97%
Dronedarone HCl	✔	95%
Gliquidone	++ Potassium channel, IC50: 27.2 nM	99%
TRAM-34	+++ IKCa1 (KCa3.1), Kd: 20 nM	98%
Glibenclamide	✔	98%
Amiodarone HCl	✔	97%
Gliclazide	++ Potassium channel, IC50: 184 nM	98%
Repaglinide	✔	98%
Dofetilide	✔	98%
Nateglinide	✔	99%
Quinine HCl dihydrate	✔	98%
ML133 HCl	+ Kir2.1, IC50: 290 nM	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。

Sophocarpine/槐果碱生物活性

描述

Sophocarpine, a natural product isolated and purified from the roots of Sophora flavescens, has a wide range of pharmacological effects.

Sophocarpine/槐果碱细胞实验

Cell Line Bone marrow-derived macrophages (BMM) Bone marrow-derived macrophages (BMM) Rat aortic endothelial cells Hepatic stellate cells Neonatal mouse cardiomyocytes (NMCMs) H9c2 cells H9c2 cells Activated hepatic stellate cells Hepatic stellate cells (HSCs)	Concentration	Treated Time	Description	References
Bone marrow-derived macrophages (BMM)	0, 0.25, 0.50, 1.00 mM	5 days	To evaluate the effect of sophocarpine on RANKL-induced osteoclast formation, results showed that sophocarpine dose-dependently suppressed osteoclast formation.	Br J Pharmacol. 2018 Mar;175(6):859-876.
Bone marrow-derived macrophages (BMM)	0.31 - 2 mM	48 or 96 h	To evaluate the cytotoxicity of sophocarpine on bone marrow-derived macrophages, results showed no toxicity up to the maximal concentration.	Br J Pharmacol. 2018 Mar;175(6):859-876.
Rat aortic endothelial cells	0.125 mmol/L	48 h	Sophocarpine suppressed AGEs-induced apoptosis in RAECs and restored the activation of MKK3/6-p38MAPK/Nrf2 antioxidative signaling pathway.	J Am Heart Assoc. 2017 Dec 2;6(12):e007441.
Hepatic stellate cells	1μM and 2μM	24 h	To study the effect of sophocarpine on LPS-stimulated hepatic stellate cells, it was found that sophocarpine significantly inhibited LPS-induced mRNA expression of PI3K, AKT, Cyto-C, Apaf1, caspase-9, and caspase-3, and reduced cell apoptosis.	Mediators Inflamm. 2018 May 16;2018:5871431.
Neonatal mouse cardiomyocytes (NMCMs)	1 mM	12 h	To assess the effect of SPC on HG-induced inflammatory responses, results showed SPC significantly inhibited the HG-induced increase in inflammatory markers	Front Pharmacol. 2019 Oct 31;10:1219.
H9c2 cells	1 mM	12 h	To assess the effect of SPC on HG-induced inflammatory responses, results showed SPC significantly inhibited the HG-induced increase in inflammatory markers	Front Pharmacol. 2019 Oct 31;10:1219.
H9c2 cells	0.01–10 mM	48 or 96 h	To assess the cytotoxicity of SPC, results showed no toxic effects of SPC on H9c2 cells up to the maximal concentration of 10 mM	Front Pharmacol. 2019 Oct 31;10:1219.
Activated hepatic stellate cells	100-1000 μg/mL	0-5 days	Sophocarpine significantly suppressed the proliferation of HSCs and down-regulated the expression of Cyclin D1 and PCNA.	World J Gastroenterol. 2014 Feb 21;20(7):1822-32.
Hepatic stellate cells (HSCs)	25, 50, 200 mg/mL	48 or 72 h	Sophocarpine inhibited the activation and proliferation of HSCs and decreased the expression of α-SMA, collagen Ⅰ and Ⅲ, TGF-β1, IL-6, TNF-α and MCP-1.	World J Gastroenterol. 2014 Feb 21;20(7):1822-32.

Cell Line

Bone marrow-derived macrophages (BMM) Bone marrow-derived macrophages (BMM) Rat aortic endothelial cells Hepatic stellate cells Neonatal mouse cardiomyocytes (NMCMs) H9c2 cells H9c2 cells Activated hepatic stellate cells Hepatic stellate cells (HSCs)

Concentration

Treated Time

Description

References

Bone marrow-derived macrophages (BMM)

0, 0.25, 0.50, 1.00 mM

5 days

To evaluate the effect of sophocarpine on RANKL-induced osteoclast formation, results showed that sophocarpine dose-dependently suppressed osteoclast formation.

Br J Pharmacol. 2018 Mar;175(6):859-876.

Bone marrow-derived macrophages (BMM)

0.31 - 2 mM

48 or 96 h

To evaluate the cytotoxicity of sophocarpine on bone marrow-derived macrophages, results showed no toxicity up to the maximal concentration.

Br J Pharmacol. 2018 Mar;175(6):859-876.

Rat aortic endothelial cells

0.125 mmol/L

48 h

Sophocarpine suppressed AGEs-induced apoptosis in RAECs and restored the activation of MKK3/6-p38MAPK/Nrf2 antioxidative signaling pathway.

J Am Heart Assoc. 2017 Dec 2;6(12):e007441.

Hepatic stellate cells

1μM and 2μM

24 h

To study the effect of sophocarpine on LPS-stimulated hepatic stellate cells, it was found that sophocarpine significantly inhibited LPS-induced mRNA expression of PI3K, AKT, Cyto-C, Apaf1, caspase-9, and caspase-3, and reduced cell apoptosis.

Mediators Inflamm. 2018 May 16;2018:5871431.

Neonatal mouse cardiomyocytes (NMCMs)

1 mM

12 h

To assess the effect of SPC on HG-induced inflammatory responses, results showed SPC significantly inhibited the HG-induced increase in inflammatory markers

Front Pharmacol. 2019 Oct 31;10:1219.

H9c2 cells

1 mM

12 h

To assess the effect of SPC on HG-induced inflammatory responses, results showed SPC significantly inhibited the HG-induced increase in inflammatory markers

Front Pharmacol. 2019 Oct 31;10:1219.

H9c2 cells

0.01–10 mM

48 or 96 h

To assess the cytotoxicity of SPC, results showed no toxic effects of SPC on H9c2 cells up to the maximal concentration of 10 mM

Front Pharmacol. 2019 Oct 31;10:1219.

Activated hepatic stellate cells

100-1000 μg/mL

0-5 days

Sophocarpine significantly suppressed the proliferation of HSCs and down-regulated the expression of Cyclin D1 and PCNA.

World J Gastroenterol. 2014 Feb 21;20(7):1822-32.

Hepatic stellate cells (HSCs)

25, 50, 200 mg/mL

48 or 72 h

Sophocarpine inhibited the activation and proliferation of HSCs and decreased the expression of α-SMA, collagen Ⅰ and Ⅲ, TGF-β1, IL-6, TNF-α and MCP-1.

World J Gastroenterol. 2014 Feb 21;20(7):1822-32.

Sophocarpine/槐果碱动物实验

Species Rat Nude mice Sprague-Dawley rats C57 BL/6 mice C57BL/6 mice BALB/C mice Rats Mice	Animal Model Rat femoral particle-induced peri-implant osteolysis model UM-SCC-22B xenograft model AGEs-induced aortic endothelial cell apoptosis model LPS-induced septic liver injury model Streptozotocin (STZ)-induced type 1 diabetes mellitus mouse model ConA-induced hepatitis model Dimethylnitrosamine (DMN) or bile duct ligation (BDL) induced liver fibrosis models Isoproterenol-induced kidney injury model	Administration	Dosage	Frequency	Description	References
Rat	Rat femoral particle-induced peri-implant osteolysis model	Intraperitoneal injection	20 mg/kg	Once daily for 12 weeks	To evaluate the effect of sophocarpine on particle-induced implant loosening, results showed that sophocarpine prevented prosthesis loosening by inhibiting osteoclast formation, resulting in reduced periprosthetic bone loss, diminished pseudomembrane formation, improved bone-implant contact, and enhanced stability of implants.	Br J Pharmacol. 2018 Mar;175(6):859-876.
Nude mice	UM-SCC-22B xenograft model	Intravenous injection	5 mg/kg	Every other day for 21 days	SC significantly inhibited tumor growth without observable tissue toxicity.	Mol Ther. 2017 Sep 6;25(9):2129-2139.
Sprague-Dawley rats	AGEs-induced aortic endothelial cell apoptosis model	Intraperitoneal injection	40 mg/kg	Once daily for 10 days	Sophocarpine alleviated AGEs-induced aortic endothelial cell apoptosis and restored the activation of MKK3/6-p38MAPK/Nrf2 antioxidative signaling pathway.	J Am Heart Assoc. 2017 Dec 2;6(12):e007441.
C57 BL/6 mice	LPS-induced septic liver injury model	Oral	30 mg/kg and 60 mg/kg	Once daily for 24 days	To investigate the protective effect of sophocarpine on LPS-induced liver injury in mice, it was found that sophocarpine significantly improved the survival rate of mice, attenuated liver injury, and reduced oxidative stress, inflammation, and apoptosis.	Mediators Inflamm. 2018 May 16;2018:5871431.
C57BL/6 mice	Streptozotocin (STZ)-induced type 1 diabetes mellitus mouse model	Intraperitoneal injection	20 mg/kg	Once daily for 16 weeks	To assess the effect of SPC on diabetes-induced cardiac dysfunction, results showed SPC significantly improved cardiac function in diabetic mice	Front Pharmacol. 2019 Oct 31;10:1219.
BALB/C mice	ConA-induced hepatitis model	Oral	30 and 60 mg/kg	Five consecutive days	Sophocarpine significantly attenuated ConA-induced hepatitis by inhibiting inflammatory mediators, chemokines, and the STAT1 signaling pathway.	Front Pharmacol. 2017 Mar 21;8:140
Rats	Dimethylnitrosamine (DMN) or bile duct ligation (BDL) induced liver fibrosis models	Intraperitoneal injection	20 mg/kg	Once daily for 3 weeks (BDL) or 4 weeks (DMN)	Sophocarpine improved liver function, reduced collagen deposition, inhibited the development of hepatic fibrosis, and down-regulated the expression of TLR4 signaling pathway-related proteins.	World J Gastroenterol. 2014 Feb 21;20(7):1822-32.
Mice	Isoproterenol-induced kidney injury model	Intraperitoneal injection	20 mg/kg and 40 mg/kg	Once daily for two weeks	Sophocarpine alleviates isoproterenol-induced kidney injury by suppressing inflammation, apoptosis, oxidative stress, and fibrosis	Molecules. 2022 Nov 15;27(22):7868

Species

Rat Nude mice Sprague-Dawley rats C57 BL/6 mice C57BL/6 mice BALB/C mice Rats Mice

Animal Model

Rat femoral particle-induced peri-implant osteolysis model UM-SCC-22B xenograft model AGEs-induced aortic endothelial cell apoptosis model LPS-induced septic liver injury model Streptozotocin (STZ)-induced type 1 diabetes mellitus mouse model ConA-induced hepatitis model Dimethylnitrosamine (DMN) or bile duct ligation (BDL) induced liver fibrosis models Isoproterenol-induced kidney injury model

Administration

Dosage

Frequency

Description

References

Rat

Rat femoral particle-induced peri-implant osteolysis model

Intraperitoneal injection

20 mg/kg

Once daily for 12 weeks

To evaluate the effect of sophocarpine on particle-induced implant loosening, results showed that sophocarpine prevented prosthesis loosening by inhibiting osteoclast formation, resulting in reduced periprosthetic bone loss, diminished pseudomembrane formation, improved bone-implant contact, and enhanced stability of implants.

Br J Pharmacol. 2018 Mar;175(6):859-876.

Nude mice

UM-SCC-22B xenograft model

Intravenous injection

5 mg/kg

Every other day for 21 days

SC significantly inhibited tumor growth without observable tissue toxicity.

Mol Ther. 2017 Sep 6;25(9):2129-2139.

Sprague-Dawley rats

AGEs-induced aortic endothelial cell apoptosis model

Intraperitoneal injection

40 mg/kg

Once daily for 10 days

Sophocarpine alleviated AGEs-induced aortic endothelial cell apoptosis and restored the activation of MKK3/6-p38MAPK/Nrf2 antioxidative signaling pathway.

J Am Heart Assoc. 2017 Dec 2;6(12):e007441.

C57 BL/6 mice

LPS-induced septic liver injury model

Oral

30 mg/kg and 60 mg/kg

Once daily for 24 days

To investigate the protective effect of sophocarpine on LPS-induced liver injury in mice, it was found that sophocarpine significantly improved the survival rate of mice, attenuated liver injury, and reduced oxidative stress, inflammation, and apoptosis.

Mediators Inflamm. 2018 May 16;2018:5871431.

C57BL/6 mice

Streptozotocin (STZ)-induced type 1 diabetes mellitus mouse model

Intraperitoneal injection

20 mg/kg

Once daily for 16 weeks

To assess the effect of SPC on diabetes-induced cardiac dysfunction, results showed SPC significantly improved cardiac function in diabetic mice

Front Pharmacol. 2019 Oct 31;10:1219.

BALB/C mice

ConA-induced hepatitis model

Oral

30 and 60 mg/kg

Five consecutive days

Sophocarpine significantly attenuated ConA-induced hepatitis by inhibiting inflammatory mediators, chemokines, and the STAT1 signaling pathway.

Front Pharmacol. 2017 Mar 21;8:140

Rats

Dimethylnitrosamine (DMN) or bile duct ligation (BDL) induced liver fibrosis models

Intraperitoneal injection

20 mg/kg

Once daily for 3 weeks (BDL) or 4 weeks (DMN)

Sophocarpine improved liver function, reduced collagen deposition, inhibited the development of hepatic fibrosis, and down-regulated the expression of TLR4 signaling pathway-related proteins.

World J Gastroenterol. 2014 Feb 21;20(7):1822-32.

Mice

Isoproterenol-induced kidney injury model

Intraperitoneal injection

20 mg/kg and 40 mg/kg

Once daily for two weeks

Sophocarpine alleviates isoproterenol-induced kidney injury by suppressing inflammation, apoptosis, oxidative stress, and fibrosis

Molecules. 2022 Nov 15;27(22):7868

Sophocarpine/槐果碱参考文献

Sophocarpine/槐果碱实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

4.06mL

0.81mL

0.41mL

20.30mL

4.06mL

2.03mL

40.59mL

8.12mL

4.06mL

Sophocarpine/槐果碱技术信息

CAS号	6483-15-4
分子式	C₁₅H₂₂N₂O
分子量	246.35
SMILES Code	O=C1C=CC[C@]2([H])[C@@]3([H])CCCN4[C@@]3([H])[C@](CCC4)([H])CN21
MDL No.	MFCD00274555

别名	13,14-Dehydromatrine
运输	蓝冰
InChI Key	AAGFPTSOPGCENQ-JLNYLFASSA-N
Pubchem ID	115269

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(202.96 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

H₂O: 10 mg/mL(40.59 mM)，配合低频超声助溶

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

配制的工作液建议现用现配，短期内尽快用完。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

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Sophocarpine/槐果碱参考文献

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Sophocarpine/槐果碱 {[allProObj[0].p_purity_real_show]}

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全球学术期刊中引用的产品

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Sophocarpine/槐果碱 参考文献

Sophocarpine/槐果碱 实验方案

Sophocarpine/槐果碱 技术信息

最近浏览的产品

大规格询价

摩尔计算器

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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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Sophocarpine/槐果碱纯度/质量文件产品仅供科研

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Sophocarpine/槐果碱生物活性

Sophocarpine/槐果碱细胞实验

Sophocarpine/槐果碱动物实验

Sophocarpine/槐果碱参考文献

Sophocarpine/槐果碱实验方案

Sophocarpine/槐果碱技术信息