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N° Cat.S2271
| Lignées cellulaires | Type dessai | Concentration | Temps dincubation | Formulation | Description de lactivité | PMID |
|---|---|---|---|---|---|---|
| MRC5 cells | Function assay | Antiviral activity against HCMV in MRC5 cells by plaque reduction assay, IC50=0.68 μM | ||||
| MRC5 cells | Proliferation assay | 10 μM | 54 hrs | Inhibition of HCMV proliferation in MRC5 cells after 54 hrs post-infection at 10 uM by plaque assay | ||
| MRC5 cells | Proliferation assay | 10 μM | 24 h | Inhibition of HCMV proliferation in MRC5 cells after 24 hrs post-infection at 10 uM by plaque assay | ||
| Bel7402 cells | Function assay | 12 h | Induction of LDLR protein in human Bel7402 cells after 12 hrs by RT-PCR assay relative to control | |||
| HepG2 cells | Function assay | 10 ug/mL | 12 h | Induction of LDLR protein expression in human HepG2 cells at 10 ug/mL after 12 hrs by flow cytometry | ||
| KB cells | Cytotoxicity assay | 72 h | Cytotoxicity against human KB cells after 72 hrs, IC50=7.32 μM | |||
| HL60 cells | Apoptosis assay | 48 hrs | Induction of apoptosis in human HL60 cells after 48 hrs using annexin V-propidium iodide staining by FACS analysis | |||
| A549 cells | Cytotoxicity assay | Cytotoxicity against human A549 cells by SRB assay, IC50=6.27 μM | ||||
| SKOV3 cells | Cytotoxicity assay | Cytotoxicity against human SKOV3 cells by SRB assay, IC50=16.44 μM | ||||
| SK-MEL-2 cells | Cytotoxicity assay | Cytotoxicity against human SK-MEL-2 cells by SRB assay, IC50=13.76 μM | ||||
| HCT15 cells | Cytotoxicity assay | Cytotoxicity against human HCT15 cells by SRB assay, IC50=16.59 μM | ||||
| CEM cells | Cytotoxicity assay | 48 hrs | Cytotoxicity against human CEM cells expressing green fluorescent protein after 48 hrs by MTT assay, CC50=2.09 μM | |||
| human CEM cells | Function assay | 7 days | Antiviral activity against 0.05 MOI Human immunodeficiency virus 1 NL4.3 infected in human CEM cells expressing green fluorescent protein assessed as p24 antigen production measured 7 days post infection by ELISA, EC50=0.13 μM | |||
| SKN cells | Growth inhibition assay | 72 h | Growth inhibition against human SKN cells after 72 hrs by MTT assay, GI50=15.88 μM | |||
| RKN cells | Growth inhibition assay | 48 hrs | Growth inhibition against human RKN cells after 48 hrs by MTT assay, GI50=49.6 μM | |||
| G402 cells | Growth inhibition assay | 48 hrs | Growth inhibition against human G402 cells after 48 hrs by MTT assay, GI50=11.87 μM | |||
| A10 cells | Function assay | 30 μM | 24 hrs | Downregulation of Scd2 mRNA expression in rat A10 cells at 30 uM after 24 hrs by quantitative RT-PCR analysis | ||
| A10 cells | Function assay | 30 μM | 24 hrs | Down regulation of Prim2 mRNA expression in rat A10 cells at 30 uM after 24 hrs by quantitative RT-PCR analysis | ||
| A10 cells | Function assay | 30 μM | 24 hrs | Downregulation of Impk mRNA expression in rat A10 cells at 30 uM after 24 hrs by quantitative RT-PCR analysis | ||
| HepG2-A16-CD81 cells | Function assay | 10 μM | NOVARTIS: Antimalarial liver stage activity measured as a greater than 50% reduction in Plasmodium yoelii schizont area in HepG2-A16-CD81 cells at 10uM compound concentration, determined by immuno-fluorescence. | |||
| HepG2-A16-CD81 cells | Function assay | 10 μM | NOVARTIS: Antimalarial liver stage activity measured as reduction in Plasmodium yoelii schizont area in HepG2-A16-CD81 cells by immuno-fluorescence, and median schizont size at 10uM compound concentration, IC50=0.548 μM | |||
| HepG2 cells | Function assay | 10 μM | 4 h | Increase in AMPKalpha phosphorylation in human HepG2 cells at 10 uM after 4 hrs by Western blot analysis relative to untreated control | ||
| HepG2 cells | Function assay | 10 μM | 4 h | Increase in total AMPKalpha level in human HepG2 cells at 10 uM after 4 hrs by Western blot analysis relative to untreated control | ||
| HepG2 cells | Function assay | 20 μM | 24 hrs | Induction of apoptosis in human HepG2 cells assessed as morphological changes at 20 uM after 24 hrs using Hoechst 33258 staining by fluorescence microscopic analysis | ||
| HT-29 cells | Cytotoxicity assay | 48 hrs | Cytotoxicity against human HT-29 cells after 48 hrs by MTT assay, IC50=8.45 μM | |||
| HepG2 cells | Cytotoxicity assay | 24 hrs | Cytotoxicity against human HepG2 cells after 24 hrs by MTT assay, IC50=11.22 μM | |||
| HepG2 cells | Cytotoxicity assay | 48 hrs | Cytotoxicity against human HepG2 cells after 48 hrs by MTT assay, IC50=8.32 μM | |||
| Cliquez pour voir plus de données expérimentales sur les lignées cellulaires | ||||||
| Poids moléculaire | 371.81 | Formule | C20H18NO4.Cl |
Stockage (À partir de la date de réception) | |
|---|---|---|---|---|---|
| N° CAS | 633-65-8 | Télécharger le SDF | Stockage des solutions mères |
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In vitro |
DMSO
: 25 mg/mL
(67.23 mM)
Water : Insoluble Ethanol : Insoluble |
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In vivo |
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Étape 1 : Entrez les informations ci-dessous (Recommandé : Un animal supplémentaire pour tenir compte des pertes pendant lexpérience)
Étape 2 : Entrez la formulation in vivo (Ceci nest que le calculateur, pas la formulation. Veuillez nous contacter dabord sil ny a pas de formulation in vivo dans la section Solubilité.)
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, ajouter ensuiteμL PEG300, mélanger et clarifier, ajouter ensuiteμL Tween 80, mélanger et clarifier, ajouter ensuite μL ddH2O, mélanger et clarifier.
Méthode de préparation de la formulation in vivo : Prendre μL DMSO liquide maître, ajouter ensuite μL Huile de maïs, mélanger et clarifier.
Remarque : 1. Assurez-vous 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 peuvent être utilisées pour faciliter la dissolution.
| Targets/IC50/Ki |
Caspase-3
Caspase-8
PARP
cytochrome c
cIAP1
Bcl-2
Bcl-xL
JNK
p38 MAPK
ROS
Topo I
Topo II
|
|---|---|
| In vitro |
Comparé au régorafénib seul, le traitement combiné de berbérine (BBR) et de régorafénib inhibe significativement la prolifération des cellules de carcinome hépatocellulaire (CHC) et induit l'apoptosis cellulaire. |
| In vivo |
Le groupe de traitement combiné avec de la berbérine (BBR) et du régorafénib a un effet inhibiteur spectaculaire sur la croissance des tumeurs de xénogreffe de carcinome hépatocellulaire (CHC) chez les souris nues. L'apoptosis accrue des tumeurs de xénogreffe est observée dans le groupe de traitement combiné. |
Références |
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(données de https://clinicaltrials.gov, mis à jour le 2024-05-22)
| Numéro NCT | Recrutement | Conditions | Sponsor/Collaborateurs | Date de début | Phases |
|---|---|---|---|---|---|
| NCT06273241 | Not yet recruiting | Pharmacokinetic Study in Healthy Volunteers |
University Medicine Greifswald |
March 4 2024 | Not Applicable |
| NCT05845931 | Recruiting | Pharmacokinetic Study in Healthy Volunteers |
University Medicine Greifswald |
May 5 2023 | Not Applicable |
| NCT05480670 | Completed | Polycystic Ovary Syndrome |
Ayub Teaching Hospital |
November 1 2022 | Not Applicable |
| NCT05463003 | Completed | Pharmacokinetic Study in Healthy Volunteers |
University Medicine Greifswald |
July 19 2022 | Not Applicable |
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