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Cat. No. | Product Name | Target | Signaling Pathways |
---|---|---|---|
T15418 |
GS-6201
CVT-6883 |
Adenosine Receptor | GPCR/G Protein; Neuroscience |
GS-6201 (CVT-6883) 是选择性腺苷 A2B 受体拮抗剂。它对人腺苷 A2B 受体具有高亲和力和选择性 (Ki=22 nM)。它降低了小鼠急性心肌梗死后心脏中 caspase-1 的活性,并减弱了心脏重塑。它减弱了致敏小鼠 NECA,AMP 或变应原诱导的气道反应性。 | |||
T7714 |
Temocapil
|
Tyrosinase | Proteases/Proteasome |
Temocapil 是一种酪氨酸激酶抑制剂。 | |||
T3230 |
NLRP3-IN-2
5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide,4-[2-(5-氯-2-甲氧基苯甲酰氨基)乙基]苯磺酰胺,NLRP3 Inflammasome Inhibitor I |
NOD-like Receptor (NLR); NOD | Immunology/Inflammation; NF-κB |
NLRP3-IN-2 (5-Chloro-N-(p-sulfamoylphenethyl)-o-anisamide) 是一种能够合成格列本脲的中间物,对心肌细胞中NLRP3炎症小体的形成具有抑制作用,在小鼠心肌缺血/再灌注后限制梗死面积,且对代谢无影响。 | |||
T6698 |
Temocapril hydrochloride
CS-622 HCl,Acecol,Temocapril HCl,CS-622,盐酸替莫普利 |
RAAS | Endocrinology/Hormones |
Temocapril hydrochloride (CS-622 HCl) 是血管紧张素转化酶 (ACE) 抑制剂。Temocapril HCl 能够用于充血性心力衰竭、急性心肌梗死、高血压、胰岛素抵抗和肾脏疾病的研究。 | |||
T0230 |
Prasugrel
LY640315,CS-747,普拉格雷,PCR 4099 |
P2Y Receptor | GPCR/G Protein; Neuroscience |
Prasugrel (CS-747) 是一种噻吩吡啶和前药,是一种可口服的 P2Y12受体拮抗剂,抑制 ADP 诱导的血小板聚集,用于预防急性冠状动脉综合征患者的血栓形成、不稳定型心绞痛和心肌梗塞,以及接受经皮冠状动脉介入治疗的患者。 | |||
T24873 |
TGX-115
TGX 115 |
PI3K | PI3K/Akt/mTOR signaling |
TGX-115是一种细胞渗透性和有效的PI 3-K 异构体p110β/p110δ抑制剂(对p110β IC50值为 0.13 μM, 对p110δ值为0.63 μM),是一种调节血小板粘附过程的酶,可抑制磷酸肌苷(PI)3-激酶,可用来治疗冠状动脉闭塞、中风、急性冠状动脉综合征、急性心肌梗塞、血管再狭窄、动脉硬化和不稳定心绞痛等心血管疾病 。 | |||
T34327 |
Ridogrel
R-70416,R 68070,R-68070,R70416,R 70416,R68070 |
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Lidogrell is a dual-acting agent that can be used to prevent systemic thromboembolism and as an adjunct to thrombolytic therapy in acute myocardial infarction. | |||
T27581 |
Icrocaptide
ITF 1697,ITF-1697,ITF1697 |
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Icrocaptide is used potentially for the treatment of acute myocardial infarction. | |||
T69078 |
Tiapamil Free Base
|
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Tiapamil Free Base is a phenylethylamine derivative that acts as a calcium antagonist showing hemodynamic effects in patients with acute myocardial infarction. | |||
T11740L |
Delcasertib acetate
KAI-9803,KID1-1,CS-9803,BMS-875944,Delcasertib acetate(949100-39-4 free base) |
PKC | Chromatin/Epigenetic; Cytoskeletal Signaling |
Delcasertib acetate 是一种选择性 δ 蛋白激酶C (δPKC) 抑制剂,可用于研究急性心肌梗死和疼痛。 | |||
T73240 |
PDE5-IN-4
|
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PDE5-IN-4为磷酸二酯酶5(PDE5)抑制剂,应用于急性心肌梗死及再灌注损伤、消化系统疾病、糖尿病相关损害及肝功能衰竭的研究。 | |||
T73661 |
Delcasertib hydrochloride
|
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Delcasertib (KAI-9803) hydrochloride 是有效,选择性的 δ 蛋白激酶 C (δPKC) 抑制剂。Delcasertib (KAI-9803) hydrochloride 可改善急性心肌梗死动物模型的缺血再灌注损伤。 | |||
T38800 |
MMPI-1154
|
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MMPI-1154 is a highly promising imidazole-carboxylic acid (ICA) MMP-2 inhibitor (IC 50 = 6.6 μM) with excellent cardio-cytoprotective properties. It is specifically designed for the study of acute myocardial infarction. Additionally, MMPI-1154 exhibits significant inhibitory effects on MMP-13, MMP-1, and MMP-9 activities with IC 50 values of 1.8 μM, 10 μM, and 13 μM, respectively. | |||
T36223 |
MitoA
|
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MitoA is a ratiometric mass spectrometry probe that can be used for assessing changes in H2S within mitochondria in vivo. MitoA contains a triphenylphosphonium cation component that drives its accumulation in mitochondria where its aryl azide moiety selectively reacts with H2S to produce an amine product, MitoN. Quantifying the MitoN/MitoA ratio by LC-MS/MS reflects the mitochondrial matrix H2S concentration. In a mouse model of acute myocardial infarction with MitoA administered prior to ischem... | |||
T83769 |
TC 14012 hydrochloride
H-Arg-Arg-Nal-Cys-Tyr-Cit-Lys-D-Cit-Pro-Tyr-Arg-Cit-Cys-Arg-NH2 |
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TC 14012是一种化学肽模拟的拮抗剂,针对趋化因子(C-X-C motif)受体4(CXCR4;IC50 = 2.9 nM)和CXCR7激动剂。它能在表达CXCR7的HEK293T细胞中诱导β-arrestin招募(EC50 = 350 nM)。TC 14012可减少HIV在MT-4细胞中的细胞病理效应(EC50 = 0.4 nM),并以CXCR4依赖的方式抑制HIV在体外进入(IC50 = 19.3 nM)。它还能抑制由趋化因子(C-X-C motif)配体12(CXCL12)在MDA-MB-231乳腺癌细胞和人脐静脉内皮细胞(HUVECs)中诱导的迁移,当使用浓度范围从10到1,000 nM时。在通过左前降(LAD)冠状动脉结扎诱导的急性心肌梗死小鼠模型中,TC 14012(10 mg/kg)能减少梗死面积。 |
Cat. No. | Product Name | Target | Signaling Pathways |
---|---|---|---|
T3S0289 |
Araloside X
|
Calcium Channel | Membrane transporter/Ion channel; Metabolism |
Aralosides possess protective effect against experimental myocardial ischemia and infarction, the mechanism of myocardial protection may be attributed to the amelioration of FFA metabolic deterioration and membrane peroxidation induced by oxygen free radi |