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Tariquidar (XR9576) P-gp Inhibitor

Name: Tariquidar (XR9576)
Brand: Selleck Chemicals
SKU: S8028
Rating: 5 (54 reviews)

Kat.-Nr.S8028

Tariquidar ist ein potenter und selektiver nichtkompetitiver Inhibitor von P-Glykoprotein mit einem K_d von 5,1 nM in der CHrB30-Zelllinie, der die Arzneimittelresistenz in MDR-Zelllinien umkehrt. Phase 3.

Tariquidar (XR9576) P-gp Inhibitor Chemical Structure

Chemische Struktur

Molekulargewicht: 646.73

Springe zu

Qualitätskontrolle

Charge: Reinheit: 99.81%

99.81

Verwandte Ziele	CFTR CRM1 CD markers AChR Calcium Channel Sodium Channel Potassium Channel GABA Receptor TRP Channel ATPase
Weitere P-gp Inhibitoren	Zosuquidar 3HCl Elacridar (GF120918) (20S)-Protopanaxadiol Solamargine Sinapine Levistilide A Evodine Valspodar Wilforine Encequidar (HM30181)

Zellkultur, Behandlung & Arbeitskonzentration

Zelllinien	Assay-Typ	Konzentration	Inkubationszeit	Aktivitätsbeschreibung	PMID
K562/DOX	Function assay	1 uM	10 mins	Inhibition of P-gp in human K562/DOX cells assessed as increase in rhodamine-123 efflux in human K562 cells at 1 uM incubated for 10 mins hrs by flow cytometry relative to untreated control	28113128
NB1643	qHTS assay			qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	29435139
SK-N-SH	qHTS assay			qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	29435139
KB-V1	Function assay	200 nM		Inhibition of P-gp in human KB-V1 cells assessed as increase in rhodamine 123 accumulation at 200 nM	21657271
SK-N-MC	qHTS assay			qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	29435139
HepG2	Cytotoxicity assay		48 hrs	Cytotoxicity against adriamycin-resistant human HepG2 cells assessed as inhibition of cell proliferation after 48 hrs by MTT assay, IC50=37.2μM	27328029
K562	Cytotoxicity assay		48 hrs	Cytotoxicity against human K562 cells after 48 hrs by MTT assay, IC50=31.56μM	28645831
K562	Cytotoxicity assay		48 hrs	Cytotoxicity against human K562 cells assessed as reduction in cell viability after 48 hrs by MTT assay, IC50=31.56μM	29631786
A2780adr	Function assay	10 uM	30 mins	Inhibition of ABCB1 in human A2780adr cells assessed as increase in accumulation of calcein AM at 10 uM preincubated for 30 mins followed by calcein AM addition measured every 60 secs for 60 mins by fluorescence assay relative to control	29547272
K562/A02	Cytotoxicity assay		48 hrs	Cytotoxicity against human K562/A02 cells overexpressing P-gp assessed as reduction in cell viability after 48 hrs by MTT assay, IC50=27.19μM	29631786
CCD-18Co	Cytotoxicity assay		48 hrs	Cytotoxicity against human CCD-18Co cells assessed as cell viability after 48 hrs by MTT assay, IC50=25μM	26197160
SW620/AD300	Cytotoxicity assay		48 hrs	Cytotoxicity against human SW620/AD300 cells assessed as cell viability after 48 hrs by MTT assay, IC50=25μM	26197160
HLF	Cytotoxicity assay		48 hrs	Cytotoxicity against HLF cells assessed as inhibition of cell proliferation after 48 hrs by MTT assay, IC50=16.69μM	27328029
CEM/VLB500	Growth inhibition assay		3 days	Growth inhibition of human CEM/VLB500 cells after 3 days by resazurin assay, GI50=13.5μM	17399990
MCF7/ADR	Cytotoxicity assay		48 hrs	Intrinsic cytotoxicity against human MCF7/ADR cells assessed as inhibition of cell proliferation after 48 hrs by MTT assay, IC50=13.1μM	27328029
HCT116	Cytotoxicity assay		48 hrs	Cytotoxicity against human HCT116 cells assessed as cell viability after 48 hrs by MTT assay, IC50=12.5μM	26197160
K562/A02	Function assay		48 hrs	Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured after 12 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=8.28μM	28645831
KBV	Function assay	5 uM	72 hrs	Reversal of P-gp-mediated drug resistance in human KBV cells assessed as potentiation of cytotoxicity by measuring IC50 at 5 uM after 72 hrs by MTT assay (Rvb = 398.34 +/- 0.58 uM), IC50=5.24μM	30384042
K562/A02	Function assay		48 hrs	Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured after 6 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=4.97μM	28645831
KBV	Function assay	10 uM	72 hrs	Reversal of P-gp-mediated drug resistance in human KBV cells assessed as potentiation of cytotoxicity by measuring IC50 at 10 uM after 72 hrs by MTT assay (Rvb = 398.34 +/- 0.58 uM), IC50=4.46μM	30384042
K562/A02	Function assay		48 hrs	Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured immediately by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=3.02μM	28645831
K562/A02	Function assay	5 uM	48 hrs	Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 at 5 uM measured after 48 hrs by MTT assay (Rvb = 43.75 to 96.91 uM), IC50=1.97μM	28645831
K562/A02	Function assay		48 hrs	Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 measured after 48 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=1.6μM	28645831
MCF-7 MX	Function assay			Inhibition of BCRP expressed in MCF-7 MX cells using Hoechst 33342 staining, IC50=1.5μM	21354800
MCF7	Function assay			Inhibition of ABCG2 in human mitoxantrone-resistant MCF7 cells by Hoechst 33342 assay, IC50=1.44544μM	18678495
HFE	Cytotoxicity assay		72 hrs	Cytotoxicity against human HFE cells assessed as cell viability after 72 hrs by MTT assay, IC50=1.28μM	26197160
MDCK	Function assay			Inhibition of BCRP expressed in MDCK cells using Hoechst 33342 staining, IC50=0.94μM	21354800
MCF7/Topo	Function assay			Inhibition of ABCG2 overexpressed in human MCF7/Topo cells by flow cytometric-based mitoxantrone efflux assay, IC50=0.916μM	19170519
MCF7/Topo	Function assay		2 hrs	Inhibition of ABCG2 in human MCF7/Topo cells after 2 hrs by Hoechst 33342 staining based fluorescence assay, IC50=0.526μM	30128080
MCF7/Topo	Function assay		2 hrs	Inhibition of ABCG2 in human MCF7/Topo cells after 2 hrs by Hoechst 33342 microplate assay, IC50=0.526μM	24900683
MCF7/Topo	Function assay			Inhibition of ABCG2 expressed in human MCF7/Topo cells by Hoechst microplate assay, IC50=0.526μM	21570282
MCF7/Topo	Function assay			Inhibition of ABCG2 in human MCF7/Topo cells by Hoechst 33342 assay, IC50=0.52μM	26774038
KBV1	Function assay		10 mins	Inhibition of ABCB1 in human KBV1 cells after 10 mins by Calcein-AM microplate assay, IC50=0.223μM	24900683
Kb-V1	Function assay		10 mins	Inhibition of ABCB1 expressed in Kb-V1 cells after 10 mins by calcein-AM assay, IC50=0.223μM	21570282
KBv1	Function assay			Inhibition of ABCB1 overexpressed in human KBv1 cells by flow cytometric-based calcein-AM efflux assay, IC50=0.223μM	19170519
KBV1	Function assay			Inhibition of ABCB1 in human KBV1 cells assessed as inhibition of calcein-AM efflux, IC50=0.22μM	26774038
A2780	Function assay		30 mins	Inhibition of human Pgp in A2780 cells after 30 mins by Hoechst 33342 assay, IC50=0.12589μM	18083034
KB-3-1	Function assay	1000 nM	72 hrs	Potentiation of doxorubicin-induced cytotoxicity against human KB-3-1 cells assessed as doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 0.15 +/- 0.04 uM), IC50=0.11μM	27504669
OVCAR8	Function assay	1000 nM	72 hrs	Potentiation of doxorubicin-induced cytotoxicity against human OVCAR8 cells assessed as doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 0.12 +/- 0.03 uM), IC50=0.08μM	27504669
A2780/ADR	Function assay			Inhibition of P-glycoprotein-mediated multidrug resistance in adriamycin-resistant human A2780/ADR cells by calcein AM assay, IC50=0.078μM	19250834
A2780adr	Function assay			Inhibition of P-gp expressed in A2780adr cells by calcein AM accumulation assay, IC50=0.08μM	21354800
A2780	Function assay			Inhibition of P-gp in human adriamycin-resistant A2780 cells by Hoechst 33342 assay, IC50=0.07244μM	18678495
KBV1	Function assay	1000 nM	72 hrs	Inhibition of human ABCB1 expressed in KBV1 cells assessed as potentiation of doxorubicin-induced cytotoxicity by measuring doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 5.07 +/- 0.19 uM), IC50=0.07μM	27504669
CEM/VLB500	Function assay		3 days	Reversal of P-gp-mediated multidrug resistance to in human CEM/VLB500 cells after 3 days by resazurin assay, EC50=0.068μM	17399990
EMT6/AR1.0	Function assay		1 hr	Inhibition of mouse Pgp in EMT6/AR1.0 cells after 1 hr by daunorubicin accumulation assay, IC50=0.06457μM	18083034
EMT6/AR1.0	Function assay		1 hr	Inhibition of mouse Pgp in EMT6/AR1.0 cells after 1 hr by daunorubicin accumulation assay, IC50=0.064μM	18083034
MDCK	Function assay		30 mins	Inhibition of P-glycoprotein (unknown origin) expressed in MDCK cells assessed as reduction of calcein-AM transport after 30 mins by fluorescence assay, EC50=0.044μM	24607999
MDCK	Function assay		30 mins	Activity at MDR1 (unknown origin) expressed in MDCK cells using calcein AM as substrate incubated for 30 mins prior to substrate addition measured after 30 mins by fluorometric analysis, EC50=0.044μM	23374872
NCI-ADR-RES	Function assay	1000 nM	72 hrs	Inhibition of human ABCB1 expressed in NCI-ADR-RES cells assessed as potentiation of cytotoxicity by measuring IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 3714.80 +/- 383.58 nM), IC50=0.01851μM	27504669
KBV1	Function assay	1000 nM	72 hrs	Inhibition of human ABCB1 expressed in KBV1 cells assessed as potentiation of cytotoxicity by measuring IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 277.68 +/- 56.61 nM), IC50=0.00066μM	27504669
HEK293	Function assay	1000 nM	72 hrs	Potentiation of doxorubicin-induced cytotoxicity against HEK293 cells assessed as doxorubicin IC50 at 1000 nM after 72 hrs by CCK8 assay (Rvb = 5.28 +/- 0.74 nM), IC50=0.00495μM	27504669
K562/A02	Cytotoxicity assay		48 hrs	Cytotoxicity against human K562/A02 cells after 48 hrs by MTT assay, IC50=27.19μM	28645831
SW620	Cytotoxicity assay		48 hrs	Cytotoxicity against human SW620 cells assessed as cell viability after 48 hrs by MTT assay, IC50=25μM	26197160
K562/A02	Function assay		48 hrs	Inhibition of ABCB1 in human K562/A02 cells assessed as potentiation of adriamycin-induced cytotoxicity by measuring ADR IC50 treated for 48 hrs followed by compound washout measured after 24 hrs by MTT assay (Rvb = 51.34 +/- 5.1 uM), IC50=14.39μM	28645831
MDCK	Function assay			Inhibition of BCRP expressed in MDCK cells by pheophorbide A assay, IC50=0.85μM	19932960
MCF7 MX	Function assay			Inhibition of BCRP expressed in MCF7 MX cells by Hoechst 33342 staining, IC50=0.68μM	19932960
NCI-ADR-RES	Function assay	1000 nM	72 hrs	Inhibition of human ABCB1 expressed in NCI-ADR-RES cells assessed as potentiation of doxorubicin-induced cytotoxicity by measuring doxorubicin IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 5.54 +/- 0.60 uM), IC50=0.24μM	27504669
MDCK	Function assay			Inhibition of MDR1 expressed in MDCK cells using rhodamine 123 staining by flow cytometry, IC50=0.21μM	21354800
CCRF-CEM/VCR1000	Function assay		240 secs	Inhibition of P-glycoprotein-mediated daunorubicin efflux from human CCRF-CEM/VCR1000 cells after 240 secs by FACS flow cytometric analysis, IC50=0.03311μM	22452412
HEK293	Function assay	1000 nM	72 hrs	Inhibition of human ABCB1 transfected in HEK293 cells assessed as potentiation of doxorubicin-induced cytotoxicity by measuring doxorubicin IC50 at 1000 nM after 72 hrs by CCK8 assay (Rvb = 504.65 +/- 44.94 nM), IC50=0.02477μM	27504669
KB-3-1	Function assay	1000 nM	72 hrs	Potentiation of cytotoxicity against human KB-3-1 cells assessed as IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 0.78 +/- 0.27 nM), IC50=0.00041μM	27504669
OVCAR8	Function assay	1000 nM	72 hrs	Potentiation of cytotoxicity against human OVCAR8 cells assessed as IC50 at 1000 nM after 72 hrs by MTT assay (Rvb = 8.53 +/- 1.95 nM), IC50=0.00518μM	27504669
MDCK	Function assay		30 mins	Activity at BCRP (unknown origin) expressed in MDCK cells using rhodamine 123 as substrate incubated for 30 mins prior to substrate addition measured after 30 mins by fluorometric analysis, EC50=0.01μM	23374872
HepG2	Function assay	10 uM	90 mins	Inhibition of P-gp mediated efflux in adriamycin-resistant human HepG2 cells assessed as intracellular rhodamine-123 accumulation at 10 uM incubated in dark condition for 90 mins by flow cytometry relative to control	27328029
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Chemische Informationen, Lagerung & Stabilität

Molekulargewicht	646.73	Formel	C₃₈H₃₈N₄O₆	Lagerung (Ab dem Eingangsdatum)	3 Jahre-20°CPulver
CAS-Nr.	206873-63-4	SDF herunterladen		Lagerung von Stammlösungen	1 Jahr-80°Cin Lösungsmittel 1 Monat-20°Cin Lösungsmittel
Synonyme	XR9576			Smiles	COC1=C(C=C2CN(CCC2=C1)CCC3=CC=C(C=C3)NC(=O)C4=CC(=C(C=C4NC(=O)C5=CC6=CC=CC=C6N=C5)OC)OC)OC

Löslichkeit

In vitro
Charge:

DMSO : 8 mg/mL (12.36 mM)
(Feuchtigkeitskontaminiertes DMSO kann die Löslichkeit verringern. Verwenden Sie frisches, wasserfreies DMSO.)

Water : Insoluble

Ethanol : Insoluble

DMSO : 15 mg/mL (23.19 mM)
(Feuchtigkeitskontaminiertes DMSO kann die Löslichkeit verringern. Verwenden Sie frisches, wasserfreies DMSO.)

Water : Insoluble

Ethanol : Insoluble

DMSO : 5.6 mg/mL (8.65 mM)
(Feuchtigkeitskontaminiertes DMSO kann die Löslichkeit verringern. Verwenden Sie frisches, wasserfreies DMSO.)

Water : Insoluble

Ethanol : Insoluble

Molaritätsrechner

Masse	Konzentration	Volumen	Molekulargewicht
=	×	×

Verdünnungsrechner Molekulargewichtsrechner

In vivo Charge:
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.
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.
Clear solution	5%DMSO 1 Corn oil Von Selleck Labs validiert. Sollten Sie Anpassungen an dieser Formulierung benötigen, kontaktieren Sie unser Verkaufsteam für kundenspezifische Tests.	0.280mg/ml (0.43mM)	Taking the 1 mL working solution as an example, add 50 μL of 5.6 mg/ml clear DMSO stock solution to 950 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results.

In-vivo-Formulierungsrechner (Klare Lösung)

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

Dosierung: mg/kg Durchschnittsgewicht der Tiere: g Dosiervolumen pro Tier:μL Anzahl der Tiere:

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

Targets/IC₅₀/Ki	P-gp (CHrB30 cells) 5.1 nM(Kd)
In vitro	Tariquidar zeigt eine hochaffine Bindung an P-gp mit einem B_max von 275 pmol/mg. Diese Verbindung zeigt eine nicht-kompetitive Interaktion mit den P-gp-Substraten. Es erhöht die Steady-State-Akkumulation dieser Zytotoxika in CH^rB30-Zellen auf Werte, die in nicht-P-gp-exprimierenden AuxB1-Zellen beobachtet werden, mit einer EC50 von 487 nM. Diese Chemikalie ist in der Lage, die Vanadat-sensitive ATPase-Aktivität von P-gp um 60-70% zu hemmen, mit potenten IC50-Werten von 43 nM. Bei höheren Konzentrationen kann es andere Resistenzmechanismen hemmen. 1 µM dieser Verbindung hebt die ABCG2 (BCRP)-vermittelte Resistenz gegen Camptothecine in vitro auf. Es verstärkt die Zytotoxizität mehrerer Medikamente, einschließlich Doxorubicin; eine vollständige Umkehr der Resistenz wird in Gegenwart von 25-80 nM dieser Chemikalie erreicht. In MC26, einer murinen Kolonkarzinom-Zelllinie mit intrinsischer Chemoresistenz, ist die Doxorubicin-IC50 in Gegenwart von 0,1 µM dieser Verbindung fünfmal niedriger (36 vs. 7 nM). In murinen Mammakarzinom-, humanen kleinzelligen Lungenkarzinom- und humanen Ovarialkarzinom-Zelllinien mit erworbener Chemotherapieresistenz (EMT6/AR1.0, H69/LX4 und 2780 AD) ist die In-vitro-Doxorubicin-IC50 in Gegenwart von 0,1 µM dieser Chemikalie 22-150-fach niedriger. Die P-gp-Hemmung bleibt 23 Stunden nach der Entfernung aus dem Kultursystem bestehen. Es stellte die Zytotoxizität von Doxorubicin im National Cancer Institute (NCI)/ADR^RES multizellulären Tumorsphäroidmodell wieder her, das von der MCF7^WT Brustkrebszelllinie abgeleitet wurde.
Kinase-Assay	Steady-State-Arzneimittelakkumulationsassay
Kinase-Assay	Zellen werden in einem Reaktionsvolumen von 1 ml für 60 min bei 37 °C unter 5% CO₂ inkubiert, um den Steady-State zu erreichen. Die Wirkung der Modulatoren XR9576 auf die [³H]-Ligandenakkumulation wird im Konzentrationsbereich von 10^-9 - 10^-6 M untersucht. Diese Verbindung wird aus einer DMSO-Stammlösung zugegeben, die eine finale Lösungsmittelkonzentration von 0,2 % (v/v) ergibt. Nach der Zellernte wird die akkumulierte Substanz mittels Flüssigszintillationszählung gemessen und auf den Zellproteingehalt normalisiert. Diagramme der akkumulierten Menge als Funktion der Modulatorkonzentration werden mit der allgemeinen Dosis-Wirkungs-Gleichung angepasst: Y={(a-b)/(1+(X/c)^d)}+b, wobei: Y=Antwort; a=Anfangsantwort; b=Endantwort; c=EC50-Konzentration; d=Steigungswert; X=Arzneimittelkonzentration.
In vivo	Tariquidar (2-8 mg/kg p.o.) verstärkt nachweislich signifikant die Antitumoraktivität von Doxorubicin (5 mg/kg, i.v.) gegen MC26-Mauskolonkarzinome in vivo. In menschlichen Karzinom-Xenotransplantaten stellte die gleichzeitige Verabreichung dieser Verbindung (6-12 mg/kg p.o.) die Antitumoraktivität gegen zwei hochresistente MDR-menschliche Tumor-Xenotransplantate (2780AD, H69/LX4) in Nacktmäusen vollständig wieder her.
Literatur	[1] https://pubmed.ncbi.nlm.nih.gov/10510451/ [2] https://pubmed.ncbi.nlm.nih.gov/14973080/ [3] https://pubmed.ncbi.nlm.nih.gov/11212278/ [4] https://pubmed.ncbi.nlm.nih.gov/14962729/

Anwendungen

Methoden	Biomarker	Bilder	PMID
Immunofluorescence	MRP7		23393594

Klinische Studieninformationen

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

NCT-Nummer	Rekrutierung	Erkrankungen	Sponsor/Kooperationspartner	Startdatum	Phasen
NCT01663545	Completed	Epilepsies Partial	National Institute of Neurological Disorders and Stroke (NINDS)\|National Institutes of Health Clinical Center (CC)	July 31 2012	--
NCT01547754	Terminated	HIV-Associated Cognitive Motor Complex	National Institute of Mental Health (NIMH)\|National Institutes of Health Clinical Center (CC)	January 9 2012	--
NCT01386476	Completed	Drug Resistance	National Institute of Mental Health (NIMH)\|National Institutes of Health Clinical Center (CC)	June 15 2011	--
NCT00082368	Completed	Cancer	National Cancer Institute (NCI)\|National Institutes of Health Clinical Center (CC)	May 16 2004	Phase 2

Technischer Support

Handhabungshinweise

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

Wenn Sie weitere Fragen haben, hinterlassen Sie bitte eine Nachricht.

Häufig gestellte Fragen

Frage 1:
Can you please give me more specific and detailed information of how to dissolve and use it (S8028) for in vivo studies?

Antwort:
It in 30% Propylene glycol, 5% Tween 80, 65% D5W at 30mg/ml will be a suspension or emulsion. If you are going to administrate this compound by oral gavage, it is fine. We also have test some vehicles for it for i.p injection, and it is soluble in 5% DMSO+45% PEG 300+ddH2O at 2mg/ml clearly. When preparing the solution, please dissolve it in DMSO clearly first, then add PEG. After they mixed well, then dilute with water.

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):