Home Metabolism COX Inhibitor Aspirin

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Aspirin COX Inhibitor

Kat.-Nr.: S3017

Aspirin ist ein Salicylat und ein irreversibler COX1- und COX2-Inhibitor, der als Analgetikum zur Linderung geringfügiger Schmerzen, als Antipyretikum zur Fiebersenkung und als entzündungshemmendes Medikament eingesetzt wird. Diese Verbindung induziert Autophagy und stimuliert mitophagy.
Aspirin COX Inhibitor Chemical Structure

Chemische Struktur

Molekulargewicht: 180.16

Springe zu

Qualitätskontrolle (Quality Control)

Charge: Reinheit: 99.99%
99.99

Zellkultur, Behandlung & Arbeitskonzentration
(Cell Culture, Treatment & Working Concentration)

Zelllinien Assay-Typ Konzentration Inkubationszeit Formulierung Aktivitätsbeschreibung 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
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Chemische Informationen, Lagerung & Stabilität (Chemical Information, Storage & Stability)

Molekulargewicht 180.16 Formel

C9H8O4

 Lagerung (Ab dem Eingangsdatum)
CAS-Nr. 50-78-2 SDF herunterladen Lagerung von Stammlösungen

Synonyme NSC 27223, Acetylsalicylic acid, ASA Smiles CC(=O)OC1=CC=CC=C1C(=O)O

Löslichkeit (Solubility)

In vitro
Charge:

DMSO : 36 mg/mL (199.82 mM)
(Feuchtigkeitskontaminiertes DMSO kann die Löslichkeit verringern. Verwenden Sie frisches, wasserfreies DMSO.)

Ethanol : 36 mg/mL

Water : Insoluble

Molaritätsrechner

Masse Konzentration Volumen Molekulargewicht
Verdünnungsrechner Molekulargewichtsrechner

In vivo
Charge:

In-vivo-Formulierungsrechner (Klare Lösung)

Schritt 1: Geben Sie die untenstehenden Informationen ein (Empfohlen: Ein zusätzliches Tier zur Berücksichtigung von Verlusten während des Experiments)

mg/kg g μL

Schritt 2: Geben Sie die In-vivo-Formulierung ein (Dies ist nur der Rechner, keine Formulierung. Bitte kontaktieren Sie uns zuerst, wenn es im Abschnitt "Löslichkeit" keine In-vivo-Formulierung gibt.)

% DMSO % % Tween 80 % ddH2O
%DMSO %

Berechnungsergebnisse:

Arbeitskonzentration: mg/ml;

Methode zur Herstellung der DMSO-Stammlösung: mg Wirkstoff vorgelöst in μL DMSO ( Konzentration der Stammlösung mg/mL, Bitte kontaktieren Sie uns zuerst, wenn die Konzentration die DMSO-Löslichkeit der Wirkstoffcharge überschreitet. )

Methode zur Herstellung der In-vivo-Formulierung: Nehmen Sie μL DMSO Stammlösung, dann hinzufügenμL PEG300, mischen und klären, dann hinzufügenμL Tween 80, mischen und klären, dann hinzufügen μL ddH2O, mischen und klären.

Methode zur Herstellung der In-vivo-Formulierung: Nehmen Sie μL DMSO Stammlösung, dann hinzufügen μL Maisöl, mischen und klären.

Hinweis: 1. Bitte stellen Sie sicher, dass die Flüssigkeit klar ist, bevor Sie das nächste Lösungsmittel hinzufügen.
2. Achten Sie darauf, das/die Lösungsmittel der Reihe nach hinzuzufügen. Sie müssen sicherstellen, dass die bei der vorherigen Zugabe erhaltene Lösung eine klare Lösung ist, bevor Sie mit der Zugabe des nächsten Lösungsmittels fortfahren. Physikalische Methoden wie Vortex, Ultraschall oder ein heißes Wasserbad können zur Unterstützung des Lösens verwendet werden.

Wirkmechanismus (Mechanism of Action)

Targets/IC50/Ki
COX2
COX1
In vitro
Aspirin hemmt die Aktivierung von NF-kappa B, verhindert so den Abbau des NF-kappa B-Inhibitors I kappa B und hält NF-kappa B somit im Zytosol zurück. Diese Verbindung hemmt auch die NF-kappa B-abhängige Transkription vom Ig kappa Enhancer und dem langen terminalen Repeat (LTR) des humanen Immundefizienzvirus (HIV) in transfizierten T-Zellen. Es und Salicylat werden teilweise durch ihre spezifische Hemmung von IKK-beta vermittelt, wodurch die Aktivierung von NF-kappaB von Genen, die an der Pathogenese der Entzündungsreaktion beteiligt sind, verhindert wird. Diese Chemikalie schützt vor Neurotoxizität, die durch die erregende Aminosäure Glutamat in primären neuronalen Kulturen und Hippocampus-Schnitten von Ratten hervorgerufen wird. Es löst die transzelluläre Biosynthese einer bisher unbekannten Klasse von Eicosanoiden während der Co-Inkubation von humanen Nabelvenenendothelzellen (HUVEC) und Neutrophilen [polymorphkernige Leukozyten (PMN)] aus. Dieses Mittel erzeugt eine einzigartige Klasse von Eicosanoiden, die durch acetylierte PGHS-2 und 5-Lipoxygenase-Interaktionen gebildet werden. Seine Behandlung hemmt die Phosphorylierung von IRS-1 an Ser307 sowie die Phosphorylierung von JNK, c-Jun und den Abbau von IkappaBalpha in 3T3-L1- und Hep G2-Zellen, die mit Tumornekrosefaktor (TNF)-alpha behandelt wurden. Diese Behandlung hemmt die Phosphorylierung von Akt und dem Säugetier-Target von Rapamycin (aber nicht der extrazellulär regulierten Kinase oder PKCzeta) als Reaktion auf TNF-alpha. Es rettet die Insulin-induzierte Glukoseaufnahme in 3T3-L1-Adipozyten, die mit TNF-alpha vorbehandelt wurden.
Literatur
  • [4] https://pubmed.ncbi.nlm.nih.gov/7568157/
  • [5] https://pubmed.ncbi.nlm.nih.gov/12714600/

Anwendungen (Applications)

Methoden Biomarker Bilder PMID
Western blot MCL-1 p-AKT / AKT / p-ERK / ERK p-AMPKα / AMPKα / p-ACC / ACC SHH / SMO / GLI1 / Bcl-2 / Foxm1
S3017-WB1
26918349
Growth inhibition assay Cell proliferation Cell viability
S3017-viability1
28446712

Klinische Studieninformationen (Clinical Trial Information)

(Daten von https://clinicaltrials.gov, aktualisiert am 2024-05-22)

NCT-Nummer Rekrutierung Erkrankungen Sponsor/Kooperationspartner Startdatum Phasen
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