SMND-309
(Synonyms: (2E)-2-[6-[(E)-2-羧基乙烯基]-2,3-二羟基苯基]-3-(3,4-二羟基苯基)丙烯酸) 目录号 : GC37653
SMND-309是丹酚酸B衍生物，对体内外的鼠皮质神经元损伤有保护作用。
Cas No.:1065559-56-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
SMND-309 is a novel derivative of salvianolic acid B, and has shown protective effects against rat cortical neuron damage in vitro and in vivo. IC50 value:Target: SMND-309 mitigated the effects of ischemia and reperfusion injury on brain by decreasing the infract volume, improving neurological function, increasing the survival of neurons and promoting angiogenesis by increasing the levels of erythropoietin (EPO), erythropoietin receptor (EPOR), phosphorylated JAK2 (P-JAK2), phosphorylated STAT3 (P-STAT3), VEGF and VEGF receptor 2 (Flk-1) in the brain.
[1]. Hou J, Tian J, Jiang W, Gao Y, Fu F. Therapeutic effects of SMND-309, a new metabolite of salvianolic acid B, on experimental liver fibrosis. Eur J Pharmacol. 2011 Jan 10;650(1):390-5. [2]. Yang J, Zhang G, Tian J, Li C, Jiang W, Xing Y, Zhu H, Hou J, Xu H, Wu J. Cardioprotective effect of SMND-309, a novel derivate of salvianolic acid B on acute myocardial infarction in rats. Basic Clin Pharmacol Toxicol. 2010 Apr;106(4):317-23. [3]. Tian J, Fu F, Li G, Wang Y, Gao Y, Liu Z, Zhang S. SMND-309, a novel derivate of salvianolic acid B, ameliorates cerebral infarction in rats: characterization and role. Brain Res. 2009 Mar 31;1263:114-21. [4]. Tian J, Li G, Zhang S, Gao Y, Jiang W, Fu F, Liu Z. SMND-309, a novel derivate of salvianolic acid B, attenuates apoptosis and ameliorates mitochondrial energy metabolism in rat cortical neurons. Basic Clin Pharmacol Toxicol. 2009 Feb;104(2):176-84. [5]. Jian Hou et al. Therapeutic effects of SMND-309, a new metabolite of salvianolic acid B, on experimental liver fibrosis European Journal of Pharmacology Volume 650, Issue 1, 10 January 2011, Pages 390-395
| Cas No. | 1065559-56-9 | SDF | |
| 别名 | (2E)-2-[6-[(E)-2-羧基乙烯基]-2,3-二羟基苯基]-3-(3,4-二羟基苯基)丙烯酸 | ||
| Canonical SMILES | OC1=C(C(/C=C/C(O)=O)=CC=C1O)/C(C(O)=O)=C\C2=CC(O)=C(C=C2)O | ||
| 分子式 | C18H14O8 | 分子量 | 358.3 |
| 溶解度 | DMSO: ≥ 3.7 mg/mL (10.33 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.791 mL | 13.9548 mL | 27.9096 mL |
| 5 mM | 0.5582 mL | 2.791 mL | 5.5819 mL |
| 10 mM | 0.2791 mL | 1.3955 mL | 2.791 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Mechanism of SMND-309 against lung injury induced by chronic intermittent hypoxia
Int Immunopharmacol 2022 Apr;105:108576.PMID:35121224DOI:10.1016/j.intimp.2022.108576.
Introduction: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common sleep disorder that causes severe physiological disturbance. Evidence showed that OSAHS is an important associated comorbidity that can affect the survival of patients with pulmonary fibrosis. Until now, the potential mechanisms by which OSAHS accelerates the progression of lung fibrosis remain unclear. By constructing a pathological model of chronic intermittent hypoxia (CIH), the present study aimed to explore the pathological progress and potential mechanism of lung injury caused by OSAHS. Meanwhile, SMND-309 was given for treatment to evaluate its potential therapeutic role in CIH-induced lung injury. Methods: Mice were randomly divided into (C57BL/6 wild-type) WT+(room air) RA, WT + CIH, SMND-309 + RA, and SMND-309 + CIH groups. The WT + CIH and SMND-309 + CIH groups were exposed to CIH condition for 12 weeks, while the other groups were processed in normal oxygen at the same time. The SMND-309 + RA and SMND-309 + CIH groups were intraperitoneally injected with SMND-309 at the last week of the modeling period. After 12 weeks of treatment, three mice from each group were perfused through the heart. Lung tissues were isolated, fixed, sectioned, and stained with H&E, Masson, and immunofluorescence stain. The rest of the lung tissues were harvested for Western blot and ELISA assays. Results: CIH treatment increased the expression of pro-inflammatory factors (TNF-α and IL-6), resulting in lung tissue structure disorder, inflammatory cell infiltration, increased pulmonary capillary permeability, and pulmonary edema. The activation of the NF-κB signaling pathway played a crucial role in the process of inflammation. Noticeably, we observed M2 macrophage accumulation in the lung after CIH exposure, which promoted epithelial-mesenchymal transition (EMT) and pulmonary tissue fibrosis. ELISA assays showed the increased expression of TGF-β, IL-10, and IL-4 in the CIH group. SMND-309 inhibited pulmonary inflammation, reduced the accumulation of M2 macrophage, alleviated collagen deposition andlung damage. Conclusion: CIH could induce chronic lung inflammation, promote the activation of M2 macrophages, trigger the occurrence of EMT, and accelerate the deposition of lung collagen, eventually leading to lung tissue damage. This study presents a possible explanation by which interstitial lung diseases, particularly idiopathic pulmonary fibrosis (IPF) with OSAHS, are usually associated with fast progress and poor prognosis. SMND-309 showed a good protective effect on CIH-induced lung damage.
SMND-309 promotes neuron survival through the activation of the PI3K/Akt/CREB-signalling pathway
Pharm Biol 2016 Oct;54(10):1982-90.PMID:26911316DOI:10.3109/13880209.2015.1137951.
Context In clinical practice, the promotion of neuron survival is necessary to recover neurological functions after the onset of stroke. Objective This study aimed to investigate the post-ischaemic neuroprotective effect of SMND-309, a novel metabolite of salvianolic acid, on differentiated SH-SY5Y cells. Materials and methods SH-SY5Y cells were differentiated by pre-treating with 5 μM all-trans-retinoic acid for 6 d. The differentiated SH-SY5Y cells were exposed to oxygen-glucose deprivation (OGD) for 2 h and reperfusion (R) for 24 h to induce OGD/R injury. After OGD injury, differentiated SH-SY5Y cells were treated with or without SMND-309 (5, 10, 20 μM) for another 24 h. Cell viability was detected through Cell counting kit-8 assay and lactate dehydrogenase leakage assay. Apoptosis was evaluated through flow cytometry, caspase-3 activity assay. Changes in protein levels were assessed through Western blot. Results SMND-309 ameliorated the degree of injury in the differentiated SH-SY5Y cells by increasing cell viabilities (5 μM, 65.4% ± 4.1%; 10 μM, 69.8% ± 3.7%; 20 μM, 75.3% ± 5.1%) and by reducing LDH activity (20 μM, 2.5 fold) upon OGD/R stimulation. Annexin V-fluorescein isothiocyanate/propidium iodide staining results suggested that apoptotic rate of differentiated SH-SY5Y cells decreased from 43.8% induced by OGD/R injury to 19.2% when the cells were treated with 20 μM SMND-309. SMND-309 significantly increased the Bcl-2 level of the injured differentiated SH-SY5Y cells but decreased the caspase-3 activity of these cells by 1.6-fold. In contrast, SMND-309 did not affect the Bax level of these cells. SMND-309 evidently increased the protein expression of BDNF when Akt and CREB were activated. This function was antagonized by the addition of LY294002. Conclusion SMND-309 can prevent neuronal cell death in vitro. This process may be related to the activation of the PI3K/Akt/CREB-signalling pathway.
SMND-309 promotes angiogenesis in human umbilical vein endothelial cells through activating erythropoietin receptor/STAT3/VEGF pathways
Eur J Pharmacol 2013 Jan 30;700(1-3):173-80.PMID:23276662DOI:10.1016/j.ejphar.2012.12.013.
The aim of the study is to investigate the direct angiogenic activities of SMND-309, a novel metabolite of salvianolic acid B, on human umbilical vein endothelial cells (HUVEC) in vitro and its potential molecular mechanisms. Effects of SMND-309 on proliferation and adhesion of HUVEC were measured using sulforhodamine B assay and cell adhesion assay kit, respectively. Effects of SMND-309 on migration and differentiation of HUVEC were examined through wound-healing assay and tube formation on matrigel method, respectively. Expressions of erythropoietin (EPO), EPO receptor, phosphorylated EPO receptor, signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3 and vascular endothelial growth factor (VEGF) were detected by Western blot. Knocking down EPO receptor gene and blocking the epidermal growth factor (EGF) receptor/Janus kinase 2 (JAK2) pathways were used to explore the potential mechanisms in SMND-309 induced angiogenesis. SMND-309 strongly induced the proliferation of HUVEC in a concentration-dependent manner within the concentrations of 1-30 μg/ml and significantly promoted the adhesion of HUVEC to different extracellular matrix at 30μg/ml. SMND-309 at doses of 3, 10, 30 μg/ml significantly enhanced the migration, capillary-like structure formation, and the levels of VEGF, phosphorylated EPO receptor and phosphorylated STAT3. Results from further experiments using HUVEC(EPO receptor-) and AG-490 showed that SMND-309 activated EPO receptor first, and then stimulated JAK2/STAT3, which up-regulated the expression of VEGF, and resulted in the angiogenesis. These results clearly show that SMND-309 has powerful angiogenic activity on HUVEC, which is mostly correlated with the up-regulation of VEGF through EPO receptor/STAT3 signal pathways.
SMND-309, a novel derivate of salvianolic acid B, ameliorates cerebral infarction in rats: characterization and role
Brain Res 2009 Mar 31;1263:114-21.PMID:19368834DOI:10.1016/j.brainres.2009.01.034.
(2E)-2-{6-[(E)-2-carboxylvinyl]-2,3-dihydroxyphenyl}-3-(3,4-dihydroxyphenyl) propenoic acid, a novel compound designated SMND-309, is a new degradation product of salvianolic acid B. The present study was conducted to evaluate whether SMND-309 has a protective effect on permanent focal cerebral ischemia in rats. The results showed that SMND-309 at doses higher than 4.0 mg/kg (i.v.) produced a significant neuroprotection in focal ischemia rats when administered 30 min after the onset of ischemia. SMND-309 (25.0 mg/kg, i.v.) demonstrated significant neuroprotective activity even after delayed administration at 1 h, 3 h and 6 h after ischemia. The neuroprotective effect of SMND-309 (25.0 mg/kg, bolus injection intravenous at 30 min after middle cerebral artery occlusion) was still present 7 days after ischemia. Meanwhile, SMND-309 significantly increased the brain ATP content, improved mitochondrial energy metabolism and mitochondrial respiratory chain complex activities and attenuated the elevation of malondialdehyde (MDA) content, the decrease in superoxide dismutase (SOD) and glutathione-peroxidase (GSH-Px) activity in brain mitochondria. All of these findings indicate that SMND-309 exerts potent and long-term neuroprotective effects with a favorable therapeutic time-window in the model of permanent cerebral ischemia, and its protective effects may be due to the amelioration of cerebral mitochondrial energy metabolism and the antioxidant property.
SMND-309, a novel derivative of salvianolic acid B, protects rat brains ischemia and reperfusion injury by targeting the JAK2/STAT3 pathway
Eur J Pharmacol 2013 Aug 15;714(1-3):23-31.PMID:23764464DOI:10.1016/j.ejphar.2013.05.043.
SMND-309 is a novel derivative of salvianolic acid B, and has shown protective effects against rat cortical neuron damage in vitro and in vivo. However the molecular mechanisms through which SMND-309 affords this protection are unclear. The present study aimed to investigate the mechanisms associated with the protective activities of SMND-309 in a cerebral ischemia and reperfusion injury rat model. In this study, we used AG490, a specific inhibitor of the signaling pathway involving the Janus Kinase 2 (JAK2)/Signal Transducers and Activators of Transcription 3 (STAT3) signaling molecules and suramin, a potent inhibitor of vascular endothelial growth factor (VEGF), to investigate the mechanisms of SMND-309. The cerebral ischemia and reperfusion injury model was induced by performing middle cerebral artery occlusion (MCAO) in the rats. SMND-309 mitigated the effects of ischemia and reperfusion injury on brain by decreasing the infract volume, improving neurological function, increasing the survival of neurons and promoting angiogenesis by increasing the levels of erythropoietin (EPO), erythropoietin receptor (EPOR), phosphorylated JAK2 (P-JAK2), phosphorylated STAT3 (P-STAT3), VEGF and VEGF receptor 2 (Flk-1) in the brain. Our results suggest that SMND-309 provides significant neuroprotective effects against cerebral ischemia and reperfusion injury. The mechanisms of this protection may be attributed to the increased VEGF expression occurring from the JAK2/STAT3 pathway, activated by the increased EPO/EPOR expression in the brain.