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Hydrocortisone (Cortisol) Glucocorticoid Receptor Agonist

Kat.-Nr.: S1696

Hydrocortison ist ein Steroidhormon oder Glucocorticoid, das von der Nebenniere produziert wird.
Hydrocortisone (Cortisol) Glucocorticoid Receptor Agonist Chemical Structure

Chemische Struktur

Molekulargewicht: 362.46

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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
mouse RAW264.7 cells Function assay 24 h Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of IFN-gamma induced NO production after 24 hrs by Griess reaction, IC50=0.061 μM 21361338
mouse L929 cells Growth inhibition assay 6 days Growth inhibition of mouse L929 cells after 6 days 926113
RAW264.7 Antiinflammatory assay Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced NO production by MTT assay, IC50 = 40.64 μM. 20879743
RAW264.7 Function assay 24 hrs Inhibition of LPS-induced nitric oxide production in mouse RAW264.7 cells after 24 hrs by Griess reaction based spectrophotometry, IC50 = 40.64 μM. 21807513
RAW264.7 Function assay 24 hrs Inhibition of LPS-induced NO production in mouse RAW264.7 cells after 24 hrs by Griess reaction, IC50 = 40.64 μM. 23067550
RAW264.7 Antiinflammatory assay 24 hrs Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production after 24 hrs by Griess assay, IC50 = 43.8 μM. 23755850
L929 Function assay 20 hrs Displacement of 1 x 10'-8 M of [1,2,3-3H]-triamcinolone acetonide from glucocorticoid receptor in soluble fraction of mouse L929 cells after 20 hrs, Kd = 0.043 μM. 926113
HEK293 Function assay Inhibition of MR-mediated transactivation of galactosidase reporter gene in HEK293 cells expressing 11betaHSD1 16759088
RAW264.7 Antiinflammatory assay 0.5 to 50 ug/ml 4 hrs Antiinflammatory activity against LPS-stimulated mouse RAW264.7 cells assessed as inhibition of IL-10 production at 0.5 to 50 ug/ml pretreated for 4 hrs followed by challenge with 1 ug/mL LPS for 48 hrs by ELISA relative to control 21384845
RAW264.7 Antiinflammatory assay 0.5 to 50 ug/ml 4 hrs Antiinflammatory activity against LPS-stimulated mouse RAW264.7 cells assessed as inhibition of IL-6 production at 0.5 to 50 ug/ml pretreated for 4 hrs followed by challenge with 1 ug/mL LPS for 48 hrs by ELISA relative to control 21384845
RAW264.7 Antiinflammatory assay 0.5 to 50 ug/ml 4 hrs Antiinflammatory activity against LPS-stimulated mouse RAW264.7 cells assessed as inhibition of IL1-beta production at 0.5 to 50 ug/ml pretreated for 4 hrs followed by challenge with 1 ug/mL LPS for 48 hrs by ELISA relative to control 21384845
RAW264.7 Antiinflammatory assay 0.5 to 50 ug/ml 4 hrs Antiinflammatory activity against LPS-stimulated mouse RAW264.7 cells assessed as inhibition of TNFalpha production at 0.5 to 50 ug/ml pretreated for 4 hrs followed by challenge with 1 ug/mL LPS for 48 hrs by ELISA relative to control 21384845
RAW264.7 Antiinflammatory assay 0.5 to 50 ug/ml 4 hrs Antiinflammatory activity against LPS-stimulated mouse RAW264.7 cells assessed as inhibition of nitric oxide production at 0.5 to 50 ug/ml pretreated for 4 hrs followed by challenge with 1 ug/mL LPS for 48 hrs by Griess reaction method relative to control 21384845
neural precursor cells Function assay Inhibition of neurosphere proliferation of mouse neural precursor cells by MTT assay 17417631
RAW264.7 Antiinflammatory assay 10 uM 2 hrs Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced increase in TNF-alpha level at 10 uM incubated for 2 hrs prior to LPS challenge measured after 22 hrs by ELISA relative to control 25515561
RAW264.7 Antiinflammatory assay 10 uM 2 hrs Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced increase in IL-6 level at 10 uM incubated for 2 hrs prior to LPS challenge measured after 22 hrs by ELISA relative to control 25515561
RAW264.7 Antiinflammatory assay 10 uM 2 hrs Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced increase in IL-1beta level at 10 uM incubated for 2 hrs prior to LPS challenge measured after 22 hrs by ELISA relative to control 25515561
RAW264.7 Antiinflammatory assay 10 uM 2 hrs Antiinflammatory activity in mouse RAW264.7 cells assessed as inhibition of LPS-induced nitric oxide production at 10 uM incubated for 2 hrs prior to LPS challenge measured after 22 hrs relative to vehicle-treated control 25515561
B16F10 Apoptosis assay 20 uM 36 hrs Induction of apoptosis in mouse B16F10 cells assessed as increase in cleaved caspase 3 level at 20 uM after 36 hrs by western blot analysis 26695732
B16F10 Apoptosis assay 20 uM 36 hrs Induction of apoptosis in mouse B16F10 cells assessed as increase in p53 expression at 20 uM after 36 hrs by propidium iodide staining based FACS analysis 26695732
B16F10 Apoptosis assay 20 uM 36 hrs Induction of apoptosis in mouse B16F10 cells assessed as increased Bax expression at 20 uM after 36 hrs by western blot analysis 26695732
B16F10 Antitumor activity assay 6.11 mg/kg Antitumor activity against mouse B16F10 cells xenografted in C57BL/J mouse assessed as inhibition of tumor growth at 6.11 mg/kg, ip 26695732
B16F10 Apoptosis assay 20 uM 36 hrs Induction of apoptosis in mouse B16F10 cells assessed as increase in cytochrome C level at 20 uM after 36 hrs by western blot analysis 26695732
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Chemische Informationen, Lagerung & Stabilität (Chemical Information, Storage & Stability)

Molekulargewicht 362.46 Formel

C21H30O5

Lagerung (Ab Erhaltdatum)
CAS-Nr. 50-23-7 SDF herunterladen Lagerung von Stammlösungen

Synonyme NSC 10483 Smiles CC12CCC(=O)C=C1CCC3C2C(CC4(C3CCC4(C(=O)CO)O)C)O

Löslichkeit (Solubility)

In vitro
Charge:

DMSO : 72 mg/mL (198.64 mM)
(Feuchtigkeitskontaminiertes DMSO kann die Löslichkeit verringern. Verwenden Sie frisches, wasserfreies DMSO.)

Ethanol : 15 mg/mL

Water : Insoluble

Molaritätsrechner

Masse Konzentration Volumen Molekulargewicht
Verdünnungsrechner Molekulargewicht-Rechner

In vivo
Charge:

In-vivo-Formulierungsrechner (Klare Lösung)

Schritt 1: Geben Sie unten die Informationen ein (Empfohlen: Ein zusätzliches Tier einplanen, um Verluste während des Experiments auszugleichen)

mg/kg g μL

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

% DMSO % % Tween 80 % ddH2O
%DMSO %

Berechnungsergebnisse:

Arbeitskonzentration: mg/ml;

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

Methode zur Herstellung der In-vivo-Formulierung: Nehmen Sie μL DMSO Stammflüssigkeit, fügen Sie als Nächstes hinzuμL PEG300, mischen und aufklären, fügen Sie als Nächstes hinzuμL Tween 80, mischen und aufklären, fügen Sie als Nächstes hinzu μL ddH2O, mischen und aufklären.

Methode zur Herstellung der In-vivo-Formulierung: Nehmen Sie μL DMSO Stammflüssigkeit, fügen Sie als Nächstes hinzu μL Maisöl, mischen und aufklären.

Hinweis: 1. Bitte stellen Sie sicher, dass die Flüssigkeit klar ist, bevor Sie das nächste Lösungsmittel hinzufügen.
2. Achten Sie darauf, die Lösungsmittel in der richtigen Reihenfolge hinzuzufügen. Sie müssen sicherstellen, dass die im vorherigen Schritt erhaltene Lösung klar ist, bevor Sie das nächste Lösungsmittel hinzufügen. Physikalische Methoden wie Vortexen, Ultraschall oder ein warmes Wasserbad können zur Unterstützung des Lösungsvorgangs verwendet werden.

Wirkungsmechanismus (Mechanism of Action)

Targets/IC50/Ki
Glucocorticoid receptor
In vitro

Hydrocortisone prevents endothelial barrier breakdown in response to pro-inflammatory stimuli (TNFalpha administration) in the human brain microvascular endothelial cell line hCMEC/D3, which could be demonstrated to be partly based on maintenance of occludin levels.

This compound-treated dendritic cells (DCs) show a decreased expression of MHC II molecules, the costimulatory molecule CD86, and the DC-specific marker CD83, as well as a strongly reduced IL-12 secretion. It inhibits production of IFN-gamma but induces an increased release of IL-4 and no change in IL-5. This chemical reduces T-cell proliferation in dendritic cells.

It prevents TNF-alpha induced severe degradation of the glycocalyx, increased coronary resistance, heightened vascular leak and permeability to hydroxyethyl starch and caused mast-cell degranulation in isolated guinea pig hearts.

This compound reduces postischemic oxidative stress, perfusion pressure, and transudate formation in isolated guinea pig hearts. It inhibits postischemic shedding of syndecan-1, heparan sulfate, and hyaluronan, as well as release of histamine from resident mast cells.

It increases the levels of IL-4-induced germ line C epsilon transcripts by twofold and delivers the signal required for transcription of mature C epsilon mRNA. This chemical induces S mu-S epsilon deletional switch recombination in IL-4-treated B cells, and support a model of sequential isotype switching from IgM to IgE via IgG4.

Referenzen
  • [4] https://pubmed.ncbi.nlm.nih.gov/18073553/
  • [5] https://pubmed.ncbi.nlm.nih.gov/8409416/

Anwendungen (Applications)

Methoden Biomarker Bilder PMID
Western blot parkin / AIMP2 CREB
S1696-WB1
28366931
Immunofluorescence Glut2
S1696-IF1
29717618
Growth inhibition assay Cell viability
S1696-viability1
22829975

Informationen zu klinischen Studien (Clinical Trial Information)

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

NCT-Nummer Rekrutierung Bedingungen Sponsor/Kollaboratoren Startdatum Phases
NCT05741762 Active not recruiting
Critical Illness|Adrenal Insufficiency|Septic Shock
Dr Adnan Agha|United Arab Emirates University
January 31 2023 --
NCT05607901 Recruiting
Dermatologic Disease
Tanta University
October 28 2022 Phase 2
NCT05324618 Completed
Atopic|Dermatitis
Ain Shams University|National Hepatology & Tropical Medicine Research Institute
May 15 2022 Phase 4