1. Immunology/Inflammation
  2. COX
    Virus Protease
  3. Aspirin

Aspirin (Synonyms: Acetylsalicylic Acid; ASA)

Cat. No.: HY-14654 Purity: 99.90%
Handling Instructions

Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2 with IC50s of 5 and 210 μg/mL.

For research use only. We do not sell to patients.

Aspirin Chemical Structure

Aspirin Chemical Structure

CAS No. : 50-78-2

Size Price Stock Quantity
Free Sample (0.5-1 mg)   Apply Now  
10 mM * 1 mL in DMSO USD 55 In-stock
Estimated Time of Arrival: December 31
500 mg USD 50 In-stock
Estimated Time of Arrival: December 31
1 g USD 60 In-stock
Estimated Time of Arrival: December 31
5 g USD 96 In-stock
Estimated Time of Arrival: December 31
10 g   Get quote  
50 g   Get quote  

* Please select Quantity before adding items.

Customer Review

Based on 5 publication(s) in Google Scholar

Other Forms of Aspirin:

Top Publications Citing Use of Products

    Aspirin purchased from MCE. Usage Cited in: Cell Death Dis. 2018 Aug 28;9(9):847.

    HIPK2 expression is upregulated by treatments with 5 μM Resveratrol, 30 μM Aspirin, 10 μM Vitamin E, and 15 μM Ursolic acid for another 16 h after the LPS treatment, as analysed by western blotting.

    View All COX Isoform Specific Products:

    • Biological Activity

    • Protocol

    • Purity & Documentation

    • References

    • Customer Review


    Aspirin is a non-selective and irreversible inhibitor of COX-1 and COX-2 with IC50s of 5 and 210 μg/mL.

    IC50 & Target[1]


    27.75 μM (IC50)


    1.17 mM (IC50)

    In Vitro

    Aspirin and other non-steroid anti-inflammatory drugs inhibit the activity of cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever[2]. Aspirin acetylates serine-530 of cyclooxygenase-1 (COX-1), thereby blocking thromboxane A synthesis in platelets and reducing platelet aggregation. This mechanism of action accounts for the effect of aspirin on prevention of coronary artery and cerebrovascular thrombosis. Aspirin is less effective in inhibiting COX-2 activity. Aspirin and salicylate inhibit COX-2 protein expression through interference with binding of CCAAT/enhancer binding protein beta (C/EBPbeta) to its cognate site on COX-2 promoter/enhancer[3]. Aspirin inhibits the activation of NF-κB. This inhibition prevents the degradation of the NF-κB inhibitor, 1κB, and therefore NF-κB is retained in the cytosol. Aspirin also inhibits NF-κB-dependent transcription from the lgκ enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells[4]. Aspirin inhibits COX-1 and COX-2 with IC50 values of 3.57 μM and 29.3 μM, respectively in human articular chondrocytes[5].

    Clinical Trial
    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : 100 mg/mL (555.06 mM; Need ultrasonic)

    H2O : 0.1 mg/mL (0.56 mM; Need ultrasonic)

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 5.5506 mL 27.7531 mL 55.5062 mL
    5 mM 1.1101 mL 5.5506 mL 11.1012 mL
    10 mM 0.5551 mL 2.7753 mL 5.5506 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.5 mg/mL (13.88 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (13.88 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.5 mg/mL (13.88 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Cell Assay

    Chondrocytes are isolated from articular cartilage of donors with no articular disease. Unstimulated and interleukin 1 (IL-1) stimulated chondrocytes are used as models to study the effects of drugs on COX-1 and COX-2. Cells are incubated with vehicle or drugs (Asprin); supernatants are removed and the level of prostaglandin E2 (PGE2) in each sample is determined by enzyme immunoassay. IC50s are calculated from the reduction in PGE2 content by different concentrations of the test substance by linear regression analysis[5].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.


    Purity: 99.90%

    • No file chosen (Maximum size is: 1024 Kb)
    • If you have published this work, please enter the PubMed ID.
    • Your name will appear on the site.
    • Molarity Calculator

    • Dilution Calculator

    The molarity calculator equation

    Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

    Mass   Concentration   Volume   Molecular Weight *
    = × ×

    The dilution calculator equation

    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

    This equation is commonly abbreviated as: C1V1 = C2V2

    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
    × = ×
    C1   V1   C2   V2


    AspirinAcetylsalicylic AcidASACOXAutophagyMitophagyVirus ProteaseCyclooxygenaseMitochondrial AutophagyInhibitorinhibitorinhibit

    Your Recently Viewed Products:

    Inquiry Online

    Your information is safe with us. * Required Fields.

    Product Name



    Applicant Name *


    Email address *

    Phone number *


    Organization name *

    Department *


    Requested quantity *

    Country or Region *



    Bulk Inquiry

    Inquiry Information

    Product Name:
    Cat. No.:
    MCE Japan Authorized Agent: