Aspirin

別名: NSC 27223, Acetylsalicylic acid, ASA 中文名稱：阿司匹林,乙酰水楊酸

目錄號：S3017 Purity: 99.99%

Aspirin (NSC 27223, Acetylsalicylic acid, ASA)是水楊酸類不可逆的COX1 and COX2抑制劑，常用作止痛藥來緩解輕微疼痛，作為解熱藥減少發(fā)熱，并作為一種抗炎藥物。Aspirin 可誘導自噬并激發(fā)線粒體自噬。

Aspirin Chemical Structure

CAS: 50-78-2

規(guī)格	價格	庫存
10mM (1mL in DMSO)	737.51	現(xiàn)貨
50mg	573.87	現(xiàn)貨
1g	5487.3	現(xiàn)貨
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產(chǎn)品質(zhì)控

批次： S301702 DMSO]36 mg/mL]false]Ethanol]36 mg/mL]false]Water]Insoluble]false 純度： 99.99%

99.99

Aspirin相關(guān)產(chǎn)品

相關(guān)靶點	COX-1 COX-2	點擊展開
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相關(guān)化合物庫	代謝化合物庫抗癌代謝化合物庫谷氨酰胺代謝化合物庫糖代謝化合物庫脂代謝化合物庫	點擊展開

細胞實驗數(shù)據(jù)示例

細胞系	實驗類型	給藥濃度	孵育時間	活性描述	文獻信息
PANC1	Growth inhibition assay	300 uM	48 hrs	Growth inhibition of human PANC1 cells at 300 uM after 48 hrs by alamar blue assay	22494617
PC3	Growth inhibition assay	300 uM	48 hrs	Growth inhibition of human PC3 cells at 300 uM after 48 hrs by alamar blue assay	22494617
SKBR3	Growth inhibition assay	300 uM	48 hrs	Growth inhibition of human SKBR3 cells at 300 uM after 48 hrs by alamar blue assay	22494617
HCT116	Function assay	1 mM	6 hrs	Inhibition of TNF-alpha-induced NF-kappaB activation in human HCT116 cells at 1 mM after 6 hrs by luciferase reporter gene assay	22154834
AGS	Function assay	15 to 60 umol/L after	12 hrs	Inhibition of Escherichia coli-stimulated IL-8 production in human AGS cells at 15 to 60 umol/L after 12 hrs by ELISA	20153183
MDA-MB-231	Function assay	100 uM	30 mins	Irreversible inhibition of COX-1 in human MDA-MB-231 cells assessed as inhibition of arachidonic acid-induced PGE2 formation at 100 uM incubated for 30 mins followed by compound washout measured 30 mins post arachidonic acid challenge by radioimmunoassay	23651359
THP1	Function assay	100 uM	30 mins	Irreversible inhibition of COX-1 in human THP1 cells assessed as inhibition of arachidonic acid-induced TXB2 formation at 100 uM incubated for 30 mins followed by compound washout measured 30 mins post arachidonic acid challenge by radioimmunoassay	23651359
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-6 in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by ELISA	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of TNF-alpha in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by E	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring reduction in MDA levels at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by spectrophotometry	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring increase in SOD activity at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by spectrophotometry	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring increase in catalase activity at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by spectrophotometry	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of TNF-alpha in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by ELISA	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-1beta in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by ELISA	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as reduction in MDA levels at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by spectrophotometry	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress in rat H9c2 cells assessed as antioxidant activity by measuring increase in SOD activity at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by spec	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-6 in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by ELISA	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced oxidative stress mediated inflammation in rat H9c2 cells assessed as suppression of IL-1beta in supernatant at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs in presence of leonurine by EL	27575471
H9c2	Cardioprotective assay	1 uM	8 hrs	Cardioprotective activity against hypoxia-induced cytotoxicity in rat H9c2 cells assessed as increase in cell viability at 1 uM preincubated for 8 hrs followed by H2O2 addition for 2 hrs by MTT assay	27575471
stem cells	Function assay	100 uM	5 days	Induction of adipogenesis in human bone marrow-derived mesenchymal stem cells assessed as increase in adiponectin production at 100 uM measured on day 5 in presence of IDX by ELISA	29398443
RPMI8226	Cell cycle assay	1.7 uM	48 hrs	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at G0/G1 phase at 1.7 uM in presence of bortezomib after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to bortezomib	30590258
RPMI8226	Cell cycle assay	1.7 uM	48 hrs	Cell cycle arrest in human RPMI8226 cells assessed as accumulation at S phase at 1.7 uM in presence of bortezomib after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to bortezomib	30590258
RPMI8226	Cell cycle assay	1.7 uM	48 hrs	Cell cycle arrest in human RPMI8226 cells assessed as reduction in accumulation at G2/M phase at 1.7 uM in presence of bortezomib after 48 hrs by propidium iodide/RNase staining based flow cytometric method relative to bortezomib	30590258
HaCaT	Antipyretic assay	100 uM	2 hrs	Antipyretic activity in human HaCaT cells assessed as inhibition of TNFalpha-induced PGE2 production at 100 uM pre-incubated for 2 hrs before TNFalpha stimulation for 24 hrs by ELISA	31393125
OVCAR5	Function assay	300 uM to 1 mM	72 hrs	Inhibition of NAPRT in human OVCAR5 cells assessed as potentiation of NAMPT inhibitor FK866-induced cytotoxicity by measuring reduction in cell viability at 300 uM to 1 mM incubated for 72 hrs by SRB assay	ChEMBL
CCRF-CEM	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human CCRF-CEM cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further	ChEMBL
Jurkat	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human Jurkat cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further i	ChEMBL
ML2	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human ML2 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further incu	ChEMBL
NOMO	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human NOMO cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further inc	ChEMBL
NB4	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human NB4 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further incu	ChEMBL
NAMALWA	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human NAMALWA cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further	ChEMBL
Daudi	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human Daudi cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further in	ChEMBL
Raji	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human Raji cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further inc	ChEMBL
ARH77	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human ARH77 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further in	ChEMBL
RPMI8226	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human RPMI8226 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further	ChEMBL
U266	Function assay	3.5 mM	48 hrs	Inhibition of NAPRT in human U266 cells assessed as potentiation of NAMPT inhibitor FK866-induced apoptosis by measuring reduction in cell viability at 3.5 mM prer-incubated with IC50 level of FK866 for 48 hrs followed by compound addition and further inc	ChEMBL
NAMALWA	Function assay	35 mg/kg	45 days	Potentiation of NAMPT inhibitor 10 mg/kg, ip bid FK866-induced antitumor activity in human NAMALWA cells xenografted in SCID mouse assessed as increase in mouse survival at 35 mg/kg, ip bid up to 45 days	ChEMBL
microglia cells	Antineuroinflammatory assay		15 mins	Antineuroinflammatory activity in LPS-stimulated rat microglia cells assessed as inhibition of PMA-stimulated TXB2 release preincubated for 15 mins measured 70 mins after PMA challenge, IC50=3.12μM	22153874
HCT116	Cytotoxicity assay		48 hrs	Cytotoxicity against human HCT116 cells assessed as reduction in cell viability after 48 hrs MTT assay	26750401
peritoneal cells	Function assay		5 hrs	Inhibition of LPS-induced PGE2 production in C57BL6 mouse peritoneal cells measured at 5 hrs time interval by ELISA, IC50=4.08μM	30006172
HCT8	Antiproliferative assay		72 hrs	Antiproliferative activity against human HCT8 cells after 72 hrs in presence of cinnamaldehyde by MTT assay, IC50=15.6μM	30037494
RAW264.7	Antiinflammatory assay			Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production by measuring nitrite accumulation by Griess method, IC50=43.2μM	28561586
DAOY	qHTS assay			qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	29435139
Rh30	qHTS assay			qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	29435139
Rh41	qHTS assay			qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	29435139
點擊查看更多細胞系數(shù)據(jù)

生物活性

產(chǎn)品描述

靶點

COX2 ^[1]

COX1 ^[1]

體外研究(In Vitro)
體外研究活性	Aspirin抑制NF-κB的活化，從而防止NF-κB抑制劑，IκB的降解，因此NF-κB保留在細胞質(zhì)中。在轉(zhuǎn)染的T細胞中，Aspirin也會抑制NF-κB依賴性Igκ增強子和人免疫缺陷病毒(HIV)長末端重復序列(LTR) 的轉(zhuǎn)錄。^[1] Aspirin和salicylate在一定程度上被它們對IKK-β的特定抑制介導，從而防止涉及炎癥反應發(fā)病機理的NF-κB基因激活。^[2]在大鼠神經(jīng)元原代培養(yǎng)物和海馬腦片中，Aspirin對興奮性氨基酸谷氨酸引發(fā)的神經(jīng)毒性具有保護作用。^[3]人臍靜脈內(nèi)皮細胞(HUVEC)和中性粒細胞[多形核白細胞(PMN)]共培養(yǎng)時，Aspirin引起一種先前未識別的類花生酸跨細胞生物合成。Aspirin引起乙酰化的PGHS-2和5-脂氧合酶相互作用形成一類獨特的類花生酸。^[4] Aspirin治療抑制IRS-1在Ser307上的磷酸化和JNK，c-Jun磷酸化，以及IkappaBalpha在腫瘤壞死因子(TNF)-α處理的3T3-L1和Hep G2細胞中的降解。Aspirin治療抑制Akt磷酸化和rapamycin (但不作用于細胞外調(diào)節(jié)激酶或PKCzeta)的哺乳動物靶點對TNF-α的響應。在TNF-α預處理的3T3-L1脂肪細胞，Aspirin減少胰島素誘導的葡萄糖攝取。^[5]
實驗圖片	檢測方法	檢測指標	實驗圖片	PMID
	Western blot	MCL-1 p-AKT / AKT / p-ERK / ERK p-AMPKα / AMPKα / p-ACC / ACC SHH / SMO / GLI1 / Bcl-2 / Foxm1		26918349
	Growth inhibition assay	Cell proliferation Cell viability		28446712

NCT Number	Recruitment	Conditions	Sponsor/Collaborators	Start Date	Phases
臨床試驗信息 (data from https://clinicaltrials.gov, updated on 2024-05-22)
NCT05960864	Not yet recruiting	Ankylosing Spondylitis (AS) / Radiographic Axial SpA (r-axSpA)\|Non-radiographic Axial Spondyloarthritis (Nr-axSpA)\|Axial Psoriatic Arthritis (axPsA)\|Acute Anterior Uveitis (AAU)\|Crohn Disease (CD)\|Ulcerative Colitis (UC)\|Reactive Arthritis (ReA)	Southwest Hospital China	September 2024	--
NCT05868525	Recruiting	Blunt Cerebrovascular Injury	Loma Linda University	July 2024	Phase 4
NCT06197009	Not yet recruiting	Axial Spondyloarthritis	Sinocelltech Ltd.	July 1 2024	Phase 2
NCT06378398	Not yet recruiting	Colorectal Neoplasia	University of Michigan Rogel Cancer Center\|National Cancer Institute (NCI)	May 2024	Early Phase 1

參考文獻
[1] Kopp E, et al. Science, 1994, 265(5174), 956-959. [2] Yin MJ, et al. Nature, 1998, 396(6706), 77-80. [3] Grilli M, et al. Science, 1996, 274(5291), 1383-1385. [4] Cl鄏ia J, et al. Proc Natl Acad Sci U S A, 1995, 92(21), 9475-9479 [5] Gao Z, et al. J Biol Chem, 2003, 278(27), 24944-24950. + 展開

參考文獻

[1] Kopp E, et al. Science, 1994, 265(5174), 956-959.
[2] Yin MJ, et al. Nature, 1998, 396(6706), 77-80.
[3] Grilli M, et al. Science, 1996, 274(5291), 1383-1385.

[4] Cl鄏ia J, et al. Proc Natl Acad Sci U S A, 1995, 92(21), 9475-9479
[5] Gao Z, et al. J Biol Chem, 2003, 278(27), 24944-24950.

+ 展開

化學信息&溶解度

分子量	180.16	分子式	C₉H₈O₄
CAS號	50-78-2	SDF	Download Aspirin SDF
Smiles	CC(=O)OC1=CC=CC=C1C(=O)O
儲存條件(自收到貨起)	3年-20°C粉狀	儲備液保存和期限建議分裝儲備液，避免反復凍融！	1年-80°C溶于溶劑
儲存條件(自收到貨起)	3年-20°C粉狀	儲備液保存和期限建議分裝儲備液，避免反復凍融！	1個月-20°C溶于溶劑

體外溶解度
批次：

DMSO : 36 mg/mL ( (199.82 mM) ；DMSO吸濕會降低化合物溶解度，請使用新開封DMSO)

Ethanol : 36 mg/mL (199.82 mM)

Water : Insoluble

摩爾濃度計算器

體內(nèi)溶解度
批次：

現(xiàn)配現(xiàn)用，請按從左到右的順序依次添加，澄清后再加入下一溶劑

動物體內(nèi)配方計算器

實驗計算

摩爾濃度計算器

質(zhì)量	濃度	體積	分子量
=	×	×

稀釋計算器分子量計算器

動物體內(nèi)配方計算器（澄清溶液）

第一步：請輸入基本實驗信息（考慮到實驗過程中的損耗，建議多配一只動物的藥量）

給藥劑量 mg/kg 動物平均體重 g 每只動物給藥體積 μL 動物數(shù)量只

第二步：請輸入動物體內(nèi)配方組成（配方適用于不溶于水的藥物；不同批次藥物配方比例不同，請聯(lián)系Selleck為您提供正確的澄清溶液配方）

% DMSO + % + % Tween 80 + % ddH2O

%DMSO+ %

計算結(jié)果：

工作液濃度： mg/ml；

DMSO母液配制方法： mg 藥物溶于μL DMSO溶液（母液濃度mg/mL，注：如該濃度超過該批次藥物DMSO溶解度，請先聯(lián)系Selleck）；

體內(nèi)配方配制方法：取μL DMSO母液，加入μL PEG300，混勻澄清后加入μL Tween 80，混勻澄清后加入μL ddH₂O，混勻澄清。

體內(nèi)配方配制方法：取μL DMSO母液，加入μL Corn oil，混勻澄清。

注意：1. 首先保證母液是澄清的；
2.一定要按照順序依次將溶劑加入，進行下一步操作之前必須保證上一步操作得到的是澄清的溶液，可采用渦旋、超聲或水浴加熱等物理方法助溶。

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C1=C0/X	C1:	LOG(C1):
C2=C1/X	C2:	LOG(C2):
C3=C2/X	C3:	LOG(C3):
C4=C3/X	C4:	LOG(C4):
C5=C4/X	C5:	LOG(C5):
C6=C5/X	C6:	LOG(C6):
C7=C6/X	C7:	LOG(C7):
C8=C7/X	C8:	LOG(C8):

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