Name: Aspirin
Brand: Selleck Chemicals
SKU: S3017
Rating: 5 (28 reviews)

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Contrôle Qualité

Lot : Pureté : 99.99%

99.99

Cibles apparentées	Dehydrogenase HSP Transferase P450 (e.g. CYP17) PDE phosphatase PPAR Vitamin Carbohydrate Metabolism Mitochondrial Metabolism
Autre COX Inhibiteurs	NS-398 (NS398) Paeoniflorin (NSC 178886) Lumiracoxib Xanthohumol Bufexamac Nimesulide Ginsenoside Rd Pranoprofen Phenacetin Tolfenamic Acid

Culture cellulaire, traitement et concentration de travail

Lignées cellulaires	Type dessai	Concentration	Temps dincubation	Description de lactivité	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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Informations chimiques, stockage et stabilité

Poids moléculaire	180.16	Formule	C₉H₈O₄	Stockage (À compter de la date de réception)	3 ans-20°Cpoudre
N° CAS	50-78-2	Télécharger le SDF		Stockage des solutions mères	1 an-80°Cen solvant 1 mois-20°Cen solvant
Synonymes	NSC 27223, Acetylsalicylic acid, ASA			Smiles	CC(=O)OC1=CC=CC=C1C(=O)O

Solubilité

In vitro
Lot:

DMSO : 36 mg/mL (199.82 mM)
(Le DMSO contaminé par lhumidité peut réduire la solubilité. Utiliser du DMSO frais et anhydre.)

Ethanol : 36 mg/mL

Water : Insoluble

Calculateur de molarité

Masse	Concentration	Volume	Poids moléculaire
=	×	×

Calculateur de dilution Calculateur de poids moléculaire

In vivo Lot:
Homogeneous suspension	CMC-NA	≥5mg/ml	Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Homogeneous suspension	CMC-NA	≥5mg/ml	Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.

Calculateur de formulation in vivo (Solution claire)

Étape 1 : Saisir les informations ci-dessous (Recommandé : Un animal supplémentaire pour tenir compte des pertes pendant lexpérience)

Dosage : mg/kg Poids moyen des animaux : g Volume de dosage par animal :μL Nombre danimaux :

Étape 2 : Saisir la formulation in vivo (Ceci est seulement le calculateur, pas la formulation. Veuillez nous contacter dabord sil ny a pas de formulation in vivo dans la section Solubilité.)

% DMSO + % + % Tween 80 + % ddH₂O

%DMSO+ %

Résultats du calcul :

Concentration de travail : mg/ml;

Méthode de préparation du liquide maître DMSO : mg médicament prédissous dans μL DMSO ( Concentration du liquide maître mg/mL, Veuillez nous contacter dabord si la concentration dépasse la solubilité du DMSO du lot de médicament. )

Méthode de préparation de la formulation in vivo : Prendre μL DMSO liquide maître, puis ajouterμL PEG300, mélanger et clarifier, puis ajouterμL Tween 80, mélanger et clarifier, puis ajouter μL ddH₂O, mélanger et clarifier.

Méthode de préparation de la formulation in vivo : Prendre μL DMSO liquide maître, puis ajouter μL Huile de maïs, mélanger et clarifier.

Note : 1. Veuillez vous assurer que le liquide est clair avant dajouter le solvant suivant.
2. Assurez-vous dajouter le(s) solvant(s) dans lordre. Vous devez vous assurer que la solution obtenue, lors de lajout précédent, est une solution claire avant de procéder à lajout du solvant suivant. Des méthodes physiques telles que le vortex, les ultrasons ou le bain-marie chaud peuvent être utilisées pour faciliter la dissolution.

Mécanisme daction

Targets/IC₅₀/Ki	COX2 COX1
In vitro	L'Aspirin inhibe l'activation de NF-kappa B, empêchant ainsi la dégradation de l'inhibiteur de NF-kappa B, I kappa B, et par conséquent NF-kappa B est retenu dans le cytosol. Ce composé inhibe également la transcription dépendante de NF-kappa B de l'enhancer Ig kappa et de la répétition terminale longue (LTR) du virus de l'immunodéficience humaine (VIH) dans les cellules T transfectées. Son action et celle du salicylate sont médiatisées en partie par leur inhibition spécifique de l'IKK-bêta, empêchant ainsi l'activation par NF-kappaB des gènes impliqués dans la pathogenèse de la réponse inflammatoire. Ce produit chimique est protecteur contre la neurotoxicité provoquée par l'acide aminé excitateur glutamate dans les cultures neuronales primaires de rat et les tranches hippocampe. Il déclenche la biosynthèse transcellulaire d'une classe d'eicosanoïdes jusqu'alors inconnue lors de co-incubation de cellules endothéliales de la veine ombilicale humaine (HUVEC) et de neutrophiles [leucocytes polymorphonucléaires (PMN)]. Cet agent évoque une classe unique d'eicosanoïdes formés par des interactions entre PGHS-2 acétylée et 5-lipoxygénase. Son traitement inhibe la phosphorylation d'IRS-1 en Ser307 ainsi que la phosphorylation de JNK, c-Jun et la dégradation d'IkappaBalpha dans les cellules 3T3-L1 et Hep G2 traitées avec le facteur de nécrose tumorale (TNF)-alpha. Ce traitement inhibe la phosphorylation d'Akt et de la cible de la rapamycine chez les mammifères (mais pas de la kinase régulée par le signal extracellulaire ni de la PKCzeta) en réponse au TNF-alpha. Il restaure l'absorption de glucose induite par l'insuline dans les adipocytes 3T3-L1 prétraités au TNF-alpha.
Références	[1] https://pubmed.ncbi.nlm.nih.gov/8052854/ [2] https://pubmed.ncbi.nlm.nih.gov/9817203/ [3] https://pubmed.ncbi.nlm.nih.gov/8910280/ [4] https://pubmed.ncbi.nlm.nih.gov/7568157/ [5] https://pubmed.ncbi.nlm.nih.gov/12714600/

Applications

Méthodes	Biomarqueurs	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

Informations sur lessai clinique

(données du https://clinicaltrials.gov, mis à jour le 2024-05-22)

Numéro NCT	Recrutement	Conditions	Promoteur/Collaborateurs	Date de début	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

Support technique

Instructions de manipulation

Tel: +1-832-582-8158 Ext:3

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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):

Aspirin COX inhibiteur

Structure chimique

Poids moléculaire: 180.16