Home Metabolism COX inhibitor - Autophagy activator - Mitophagy activator Aspirin For research use only.

Aspirin

Synonyms: NSC 27223, Acetylsalicylic acid, ASA

Aspirin is a salicylate, and irreversible COX1 and COX2 inhibitor, used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. Aspirin induces autophagy and stimulates mitophagy.

Aspirin Chemical Structure

Aspirin Chemical Structure

CAS No. 50-78-2

Purity & Quality Control

Aspirin Related Products

Signaling Pathway

COX Signaling Pathways

COX Signaling Pathway

Cell Data

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
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
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 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
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
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
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
HCT116 Cytotoxicity assay 48 hrs Cytotoxicity against human HCT116 cells assessed as reduction in cell viability after 48 hrs MTT assay 26750401
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
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
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
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
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
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
Click to View More Cell Line Experimental Data

Biological Activity

Description Aspirin is a salicylate, and irreversible COX1 and COX2 inhibitor, used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. Aspirin induces autophagy and stimulates mitophagy.
Targets
COX2 [1] COX1 [1]
In vitro
In vitro Aspirin inhibits the activation of NF-kappa B, thus prevents the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B is retained in the cytosol. Aspirin also inhibits NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells. [1] Aspirin and salicylate are mediated in part by their specific inhibition of IKK-beta, thereby preventing activation by NF-kappaB of genes involved in the pathogenesis of the inflammatory response. [2] Aspirin is protective against neurotoxicity elicited by the excitatory amino acid glutamate in rat primary neuronal cultures and hippocampal slices. [3] Aspirin triggers transcellular biosynthesis of a previously unrecognized class of eicosanoidsduring coincubations of human umbilical vein endothelial cells (HUVEC) and neutrophils [polymorphonuclear leukocytes (PMN)]. Aspirin evokes a unique class of eicosanoids formed by acetylated PGHS-2 and 5-lipoxygenase interactions. [4] Aspirin treatment inhibits the phosphorylation of IRS-1 at Ser307 as well as the phosphorylation of JNK, c-Jun, and degradation of IkappaBalpha in 3T3-L1 and Hep G2 cells treated with tumor necrosis factor (TNF)-alpha. Aspirin treatment inhibits phosphorylation of Akt and the mammalian target of rapamycin (but not extracellular regulated kinase or PKCzeta) in response to TNF-alpha. Aspirin rescues insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. [5]
Experimental Result Images Methods Biomarkers Images 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
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

Chemical Information & Solubility

Molecular Weight 180.16 Formula

C9H8O4
CAS No. 50-78-2 SDF Download Aspirin SDF
Smiles CC(=O)OC1=CC=CC=C1C(=O)O
Storage (From the date of receipt)

In vitro
Batch:

DMSO : 36 mg/mL ( (199.82 mM) Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 36 mg/mL

Water : Insoluble


Molecular Weight Calculator

In vivo
Batch:

Add solvents to the product individually and in order.


In vivo Formulation Calculator

Preparing Stock Solutions

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)

mg/kg g μL

Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Calculation results:

Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such
as vortex, ultrasound or hot water bath can be used to aid dissolving.

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.

* Indicates a Required Field

Please enter your name.
Please enter your email. Please enter a valid email address.
Please write something to us.
Tags: buy Aspirin | Aspirin supplier | purchase Aspirin | Aspirin cost | Aspirin manufacturer | order Aspirin | Aspirin distributor