Acetyl-Calpastatin(184-210)(human) TFA 是一种有效，选择性和可逆的钙蛋白酶 (calpain) 抑制剂，对 μ-钙蛋白酶和组织蛋白酶 L 的 Ki 值分别为 0.2 nM 和 6 μM。
Acetyl-Calpastatin(184-210)(human) TFA Chemical Structure
规格
是否有货
100 mg
;
询价
;
250 mg
;
询价
;
500 mg
;
询价
;
* Please select Quantity before adding items.
生物活性
Acetyl-Calpastatin(184-210)(human) TFA is a potent, selective and reversible calpain inhibitor with Ki values of 0.2 nM and 6 μM for µ-calpain and cathepsin L, respectively[1][2].
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent Solubility
In Vitro:;
H2O
Peptide Solubility and Storage Guidelines:
1.;;Calculate the length of the peptide.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. Ferdinando Fiorino, et al. A new cell-permeable calpain inhibitor. J Pept Sci. 2007 Jan;13(1):70-3.
[2]. Benjamin P Davis, et al. Eosinophilic esophagitis-linked calpain 14 is an IL-13-induced protease that mediates esophageal epithelial barrier impairment. JCI Insight. 2016 Apr;1(4):e86355.
N-Acetyl-Ser-Asp-Lys-Pro acetate Chemical Structure
规格
价格
是否有货
数量
1 mg
￥500
In-stock
5 mg
￥1000
In-stock
10 mg
￥1750
In-stock
25 mg
￥3800
In-stock
50 mg
;
询价
;
100 mg
;
询价
;
* Please select Quantity before adding items.
N-Acetyl-Ser-Asp-Lys-Pro acetate 相关产品
bull;相关化合物库:
Bioactive Compound Library Plus
Immunology/Inflammation Compound Library
Metabolism/Protease Compound Library
Angiogenesis Related Compound Library
Peptide Library
生物活性
N-Acetyl-Ser-Asp-Lys-Pro (Ac-SDKP) acetate is a specific substrate for the N-terminal active site of angiotensin-converting enzyme (ACE). N-Acetyl-Ser-Asp-Lys-Pro acetate is a natural inhibitor of pluripotent hematopoietic stem cell proliferation. Anti-inflammatory and antifibrotic properties[1][2].
分子量
547.56
Formula
C22H37N5O11
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Peng H, et al. Ac-SDKP reverses cardiac fibrosis in rats with renovascular hypertension. Hypertension. 2003;42(6):1164-1170.
[2]. Sharma U, et al. Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage. Am J Physiol Heart Circ Physiol. 2008;294(3):H1226-H1232.
Acetyl-Hirudin (54-65) (sulfated) 直接与凝血酶-rHCII(L444R) 结合，破坏 rHCII 的 N 末端酸性结构域与凝血酶的阴离子结合异位点 I 之间的相互作用，有助于稳定复合物。
Acetyl-Hirudin (54-65) (sulfated) Chemical Structure
CAS No. : 125441-00-1
规格
是否有货
100 mg
;
询价
;
250 mg
;
询价
;
500 mg
;
询价
;
* Please select Quantity before adding items.
生物活性
Acetyl-Hirudin (54-65) (sulfated) binds directly to thrombin-rHCII(L444R) and disrupts interactions between the N-terminal acidic domain of rHCII and anion-binding exosite I of thrombin that serves to stabilize the complex[1].
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent Solubility
In Vitro:;
H2O
Peptide Solubility and Storage Guidelines:
1.;;Calculate the length of the peptide.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. J H Han, et al. Heparin facilitates dissociation of complexes between thrombin and a reactive site mutant (L444R) of heparin cofactor II. J Biol Chem. 1997 Mar 28;272(13):8243-9.
Acetyl tetrapeptide-15 is a synthetic peptide used in the cosmetics for sensitive skin. Acetyl tetrapeptide-15 is derived from endomorphin-2 (Tyr-Pro-Phe-Phe-NH2), a human μ-opioid agonist with selective anti-nociceptive effect. Acetyl tetrapeptide-15 reduces skin hyperreactivity producing inflammatory, chronic and neuropathic pain, by increasing the threshold of neuronal excitability in μ-opioid receptor via an endorphin-like pathway[1].
分子量
613.70
Formula
C34H39N5O6
CAS 号
928007-64-1
运输条件
Room temperature in continental US; may vary elsewhere.
Acetyl-Calpastatin(184-210)(human) 是一种有效，选择性和可逆的钙蛋白酶 (calpain) 抑制剂，对 μ-钙蛋白酶和组织蛋白酶 L 的 Ki 值分别为 0.2 nM 和 6 μM。
Acetyl-Calpastatin(184-210)(human) Chemical Structure
CAS No. : 123714-50-1
规格
是否有货
100 mg
;
询价
;
250 mg
;
询价
;
500 mg
;
询价
;
* Please select Quantity before adding items.
生物活性
Acetyl-Calpastatin(184-210)(human) is a potent, selective and reversible calpain inhibitor with Ki values of 0.2 nM and 6 μM for µ-calpain and cathepsin L, respectively[1][2].
体外研究 (In Vitro)
Acetyl-Calpastatin(184-210)(human) (peptide 1; 12.5-100 μM) inhibits calpains in LCLC 103H cells with an IC50 of 27 μM[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent Solubility
In Vitro:;
H2O
Peptide Solubility and Storage Guidelines:
1.;;Calculate the length of the peptide.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. Ferdinando Fiorino, et al. A new cell-permeable calpain inhibitor. J Pept Sci. 2007 Jan;13(1):70-3.
[2]. Benjamin P Davis, et al. Eosinophilic esophagitis-linked calpain 14 is an IL-13-induced protease that mediates esophageal epithelial barrier impairment. JCI Insight. 2016 Apr;1(4):e86355.
Argireline acetate (Acetyl hexapeptide-3 acetate) is a non-toxic, skin-permeable, antiwrinkle peptide. Argireline acetate significantly inhibits Ca2+ dependent neurotransmitter release (acetylcholine) at the neuromuscular junction. Argireline acetate has antiwrinkle and anti-aging activity[1][2][3].
体外研究 (In Vitro)
The incubation of Argireline solution in different concentrations with human embryonic kidney HEK-293 (IC50 of 34.862 μM) and neuroblastoma IMR-32 cells (IC50 of 68.458 μM)) for 48 h have dose dependent antiproliferative effect. Argireline solution incubated in different concentrations with HSF has a dose-dependent antiproliferative effect on those cells. Cellular proliferation is not effected in Argireline low concentration[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Argireline is applied to the aged mice twice daily for 6 weeks. There is an improvement in the histological structure of skin tissue in the aged mice; the amount of type I collagen fibers increased, while that of type III collagen fibers decreased. Argireline could improve the histological structure of skin tissue and rejuvenate the aging skin[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
949.04
Formula
C36H64N14O14S
Sequence
N-acetyl-Glu-Glu-Met-Gln-Arg-Arg-NH2
Sequence Shortening
Ac-EEMQRR-NH2
中文名称
醋酸阿基瑞林
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Blanes-Mira C, et al. A synthetic hexapeptide (Argireline) with antiwrinkle activity. Int J Cosmet Sci. 2002 Oct;24(5):303-10.
[2]. Grosicki M, et al. The study of cellular cytotoxicity of argireline – an anti-aging peptide. Acta Biochim Pol. 2014;61(1):29-32.
[3]. Wang Y, et al. The anti-wrinkle efficacy of Argireline. J Cosmet Laser Ther. 2013 Aug;15(4):237-41.
Acetyl-pepstatin is a potent classical inhibitor of aspartic proteases (PRs) with XMRV PR and HIV-1 PR Ki values of 712 nM and 13 nM[1].
IC50 Target
Ki: 13 nM (XMRV PR) and 712 nM (XMRV PR)[1]
分子量
643.81
Formula
C31H57N5O9
CAS 号
11076-29-2
中文名称
乙酰胃泌素
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent Solubility
In Vitro:;
H2O
Peptide Solubility and Storage Guidelines:
1.;;Calculate the length of the peptide.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. Matúz K, et al. Inhibition of XMRV and HIV-1 proteases by pepstatin A and acetyl-pepstatin. FEBS J. 2012;279(17):3276-3286.
N-Acetyl-Ser-Asp-Lys-Pro, an endogenous tetrapeptide secreted by bone marrow, is a specific substrate for the N-terminal site of ACE.
体外研究 (In Vitro)
N-Acetyl-Ser-Asp-Lys-Pro is degraded specifically by ACE, and its plasma level rises substantially during ACE inhibitor therapy. Flow cytometry of rat cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro shows significant inhibition of the progression of cells from G0/G1 phase to S phase of the cell cycle. Moreover, phosphorylation and nuclear translocation of Smad2 is decreased in cardiac fibroblasts treated with N-Acetyl-Ser-Asp-Lys-Pro[1]. N-acetyl-seryl-aspartyl-lysyl-proline appears to exert this function by blocking the action of a stem cell-specific proliferation stimulator and acts selectively on quiescent progenitors[2]. N-Acetyl-Ser-Asp-Lys-Pro inhibits collagenase expression and activation is associated with increased expression of TIMP-1 and TIMP-2. N-Acetyl-Ser-Asp-Lys-Pro normalizes the IL-1β-mediated increase in MMP-2 and MMP-9 activities and MMP-13 expression[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
N-Acetyl-Ser-Asp-Lys-Pro prevents hypertension-induced inflammatory cell infiltration, collagen deposition, nephrin downregulation and albuminuria, which could lead to renoprotection in hypertensive mice[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
487.50
Formula
C20H33N5O9
CAS 号
127103-11-1
Sequence
Ac-Ser-Asp-Lys-Pro
Sequence Shortening
Ac-SDKP
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Rousseau A, et al. The hemoregulatory peptide N-acetyl-Ser-Asp-Lys-Pro is a natural and specificsubstrate of the N-terminal active site of human angiotensin-converting enzyme. J Biol Chem. 1995 Feb 24;270(8):3656-61.
[2]. Pokharel S, et al. N-acetyl-Ser-Asp-Lys-Pro inhibits phosphorylation of Smad2 in cardiac fibroblasts. Hypertension. 2002 Aug;40(2):155-61.
[3]. Rhaleb NE, et al. N-acetyl-Ser-Asp-Lys-Pro inhibits interleukin-1β-mediated matrix metalloproteinase activation in cardiac fibroblasts. Pflugers Arch. 2013 Oct;465(10):1487-95.
[4]. Rhaleb NE, et al. Renal protective effects of N-acetyl-Ser-Asp-Lys-Pro in deoxycorticosterone acetate-salt hypertensive mice. J Hypertens. 2011 Feb;29(2):330-8.
AKBA (Acetyl-11-keto-β-boswellic acid) is an active triterpenoid compound from the extract of Boswellia serrate and a novel Nrf2 activator.
IC50 & Target
Human Endogenous Metabolite
体外研究 (In Vitro)
AKBA (Acetyl-11-keto-β-boswellic acid) significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE)[1]. AKBA (Acetyl-11-keto-β-boswellic acid) significantly inhibited human colon adenocarcinoma growth, showing arrest of the cell cycle in G1-phase and induction of apoptosis[3]. AKBA (Acetyl-11-keto-β-boswellic acid) triggered significant lipolysis in 3T3-L1 adipocytes as shown by reduced neutral lipids in cytosol and increased free fatty acids in culture medium. Increased lipolysis by AKBA was accompanied by up-regulation of lipolytic enzymes, adipocyte triglyceride lipase (ATGL) and hormone sensitive lipase (HSL), and a decreased expression of lipid droplet stability regulator perilipin. In addition, AKBA (Acetyl-11-keto-β-boswellic acid) treatment reduced phenotypic markers of mature adipocyte aP2, adiponectin and glut-4 in mature adipocytes[5].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
AKBA (Acetyl-11-keto-β-boswellic acid) significantly prevented the formation of intestinal adenomatous polyps without toxicity to mice. AKBA’s activity both in the prevention of small intestinal and colonic polyps was more potently than aspirin. Histopathologic examination revealed that AKBA’s effect, that is the reduction of polyp size and degree of dysplasia, was more prominent in larger sized polyps, especially those originating in colon[1]. AKBA (Acetyl-11-keto-β-boswellic acid) administration in mice effectively delayed the growth of HT-29 xenografts without signs of toxicity. The activity of AKBA was more potent than that of aspirin[3]. AKBA (Acetyl-11-keto-β-boswellic acid) exhibited anti-cancer activity in vitro and in vivo. With oral application in mice, AKBA significantly inhibited SGC-7901 and MKN-45 xenografts without toxicity[4].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
512.72
Formula
C32H48O5
CAS 号
67416-61-9
中文名称
3-乙酰基-11-酮基-β-乳香酸
运输条件
Room temperature in continental US; may vary elsewhere.
Barlerin (8-O-Acetyl shanzhiside methyl ester) is an iridoid glucoside isolated from the leaves of Lamiophlomis rotata Kudo, a Chinese folk medicinal plant in Xi-zang. Barlerin (8-O-Acetyl shanzhiside methyl ester) could inhibt NF-κB.
IC50 & Target[1]
NF-κB
体外研究 (In Vitro)
Treatment of SH-SY5Y cells with Barlerin (8-O-Acetyl shanzhiside methyl ester) blocks TNF-α-induced nuclear transcription factor κB (NF-κB) activation and decreases high-mobility group box-1 (HMGB-1) expression. [1]. Treatment of H9c2 cells with Barlerin (8-O-Acetyl shanzhiside methyl ester) 9 μM blocks TNF-α-induced NF-κB phosphorylation by blocking High-mobility group box1 (HMGB1) expression[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
Barlerin (8-O-Acetyl shanzhiside methyl ester) 40 mg/kg demonstrates significant neuroprotective effect even after delayed administration at 4 hr after I/R. Barlerin 40 mg/kg attenuates the histopathological damage, decreases brain swelling, inhibits NF-κB activation and reduces HMGB-1 expression in ischaemic brain tissue[1]. Barlerin (8-O-Acetyl shanzhiside methyl ester) significantly promotes angiogenesis in the ischaemic brain and improves functional outcome after stroke. Barlerin also significantly increases vascularization compared with vehicle treatment. It increases the expression of VEGF, Ang1, phosphorylation of Tie2 and Akt VEGF[3]. Barlerin (8-O-Acetyl shanzhiside methyl ester) significantly shortens capillary blood clotting time and reduces blood loss volume, but does not influence mice activated partial thromboplastin time, prothrombin time or thrombin time. It significantly prolongs euglobulin clot lysis time in hyperfibrinolysis mice[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
448.42
Formula
C19H28O12
CAS 号
57420-46-9
中文名称
8-O-乙酰山栀苷甲酯
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Zhang L, et al. 8-O-acetyl shanzhiside methylester attenuates cerebral ischaemia/reperfusion injury through an anti-inflammatory mechanism in diabetic rats. Basic Clin Pharmacol Toxicol. 2014 Dec;115(6):481-7.
[2]. Kang ZC, et al. Cardioprotection with 8-O-acetyl shanzhiside methylester on experimental myocardial ischemia injury. Eur J Pharm Sci. 2012 Aug 30;47(1):124-30.
[3]. Jiang WL, et al. Effect of 8-O-acetyl shanzhiside methylester increases angiogenesis and improves functional recovery after stroke. Basic Clin Pharmacol Toxicol. 2011 Jan;108(1):21-7.
[4]. Fan PC, et al. A new anti-fibrinolytic hemostatic compound 8-O-acetyl shanzhiside methylester extracted from Lamiophlomis rotata. J Ethnopharmacol. 2016 Jul 1;187:232-8.
Cell Assay [2]
Prior to hypoxia, cells are pretreated with various concentrations (1, 3, 9 and 27μM) of Barlerin (8-O-Acetyl shanzhiside methyl ester) for 24 h. Cell viability are determined by MTT assay[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [3][4]
Rats: Barlerin (8-O-Acetyl shanzhiside methyl ester) is prepared in saline. Adult male rats are subjected to 1 hr of middle cerebral artery occlusion (MCAO) and reperfusion, and treated with or without different doses (5 and 10 mg/kg) of ND01, starting 24 hr after ischaemia and reperfusion (I/R) and by intravenous injection daily for 14 days. Neurological functional tests are performed and cerebral Evans blue extravasation is measured[3].
Mouse: Barlerin (8-O-Acetyl shanzhiside methyl ester) is prepared in saline. Male Balb/C mice (20 to 25g) are randomly divided into five groups (saline group, Hemocoagulase, 0.34 KU/kg, i.v. ASM-L, 100 mg/kg, i.v., ASM-M, 250 mg/kg, i.v., ASM-H, 500 mg/kg, i.v.). The drugs and vehicle are injected through vena caudal is 5 min before anesthetized with sodium pentobarbital (200 mg/kg, i.p.). Twenty minutes after injection, blood are drawn from heart. Activated partial thromboplastin time, prothrombin time, thrombin time and fibrinogen are assayed[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Zhang L, et al. 8-O-acetyl shanzhiside methylester attenuates cerebral ischaemia/reperfusion injury through an anti-inflammatory mechanism in diabetic rats. Basic Clin Pharmacol Toxicol. 2014 Dec;115(6):481-7.
[2]. Kang ZC, et al. Cardioprotection with 8-O-acetyl shanzhiside methylester on experimental myocardial ischemia injury. Eur J Pharm Sci. 2012 Aug 30;47(1):124-30.
[3]. Jiang WL, et al. Effect of 8-O-acetyl shanzhiside methylester increases angiogenesis and improves functional recovery after stroke. Basic Clin Pharmacol Toxicol. 2011 Jan;108(1):21-7.
[4]. Fan PC, et al. A new anti-fibrinolytic hemostatic compound 8-O-acetyl shanzhiside methylester extracted from Lamiophlomis rotata. J Ethnopharmacol. 2016 Jul 1;187:232-8.
