CP 100356 hydrochlorideP-gp inhibitor CAS# 142715-48-8 |
- 3,3'-Diindolylmethane
Catalog No.:BCC1306
CAS No.:1968-05-4
- BAM7
Catalog No.:BCC1397
CAS No.:331244-89-4
- Bendamustine HCl
Catalog No.:BCC1153
CAS No.:3543-75-7
- Betulinic acid
Catalog No.:BCN5524
CAS No.:472-15-1
- Brassinolide
Catalog No.:BCC1438
CAS No.:72962-43-7
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 142715-48-8 | SDF | Download SDF |
PubChem ID | 71312025 | Appearance | Powder |
Formula | C31H37ClN4O6 | M.Wt | 597.1 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 20 mM in DMSO | ||
Chemical Name | 4-(6,7-dimethoxy-3,4-dihydro-1H-isoquinolin-2-yl)-N-[2-(3,4-dimethoxyphenyl)ethyl]-6,7-dimethoxyquinazolin-2-amine;hydrochloride | ||
SMILES | COC1=C(C=C(C=C1)CCNC2=NC3=CC(=C(C=C3C(=N2)N4CCC5=CC(=C(C=C5C4)OC)OC)OC)OC)OC.Cl | ||
Standard InChIKey | WWCHXVYTCMPAMV-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C31H36N4O6.ClH/c1-36-24-8-7-19(13-25(24)37-2)9-11-32-31-33-23-17-29(41-6)28(40-5)16-22(23)30(34-31)35-12-10-20-14-26(38-3)27(39-4)15-21(20)18-35;/h7-8,13-17H,9-12,18H2,1-6H3,(H,32,33,34);1H | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | High affinity P-glycoprotein (P-gp) inhibitor (Ki values are 58 and 94 nM for mouse Pgp1a and Pgp1b isoforms). Inhibits calcein-AM uptake in MDR1-transfected MDCKII cells (IC50 = 0.5 μM) and prazosin transport in BCRP-transfected MDCKII cells (IC50 = 1.5 μM). Displays weak or no inhibitory activity against MRP1, OATP1B1 and several major human P450 enzymes (IC50 > 50 μM). |
CP 100356 hydrochloride Dilution Calculator
CP 100356 hydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.6748 mL | 8.3738 mL | 16.7476 mL | 33.4952 mL | 41.869 mL |
5 mM | 0.335 mL | 1.6748 mL | 3.3495 mL | 6.699 mL | 8.3738 mL |
10 mM | 0.1675 mL | 0.8374 mL | 1.6748 mL | 3.3495 mL | 4.1869 mL |
50 mM | 0.0335 mL | 0.1675 mL | 0.335 mL | 0.6699 mL | 0.8374 mL |
100 mM | 0.0167 mL | 0.0837 mL | 0.1675 mL | 0.335 mL | 0.4187 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
- Macrocarpal B
Catalog No.:BCN6236
CAS No.:142698-60-0
- Genkwanol B
Catalog No.:BCN8013
CAS No.:142674-67-7
- 6-Hydroxykaempferol 3,6-diglucoside
Catalog No.:BCN3335
CAS No.:142674-16-6
- Macrocarpal D
Catalog No.:BCN6235
CAS No.:142647-71-0
- Macrocarpal E
Catalog No.:BCN6234
CAS No.:142628-54-4
- Macrocarpal C
Catalog No.:BCN6233
CAS No.:142628-53-3
- Daphylloside
Catalog No.:BCN6232
CAS No.:14260-99-2
- Deacetylasperulosidic acid
Catalog No.:BCN3323
CAS No.:14259-55-3
- Didymin
Catalog No.:BCN3327
CAS No.:14259-47-3
- Narirutin
Catalog No.:BCN6300
CAS No.:14259-46-2
- Asperuloside
Catalog No.:BCN6231
CAS No.:14259-45-1
- Calanolide E
Catalog No.:BCN6230
CAS No.:142566-61-8
- Dihydrocurcumenone
Catalog No.:BCN3557
CAS No.:142717-57-5
- FGIN-1-27
Catalog No.:BCC6738
CAS No.:142720-24-9
- Conophylline
Catalog No.:BCN6237
CAS No.:142741-24-0
- Buddlenoid A
Catalog No.:BCN8210
CAS No.:142750-32-1
- Anemarsaponin BIII
Catalog No.:BCN2898
CAS No.:142759-74-8
- 12-Hydroxysapriparaquinone
Catalog No.:BCN3216
CAS No.:142763-37-9
- Domoic acid
Catalog No.:BCC6586
CAS No.:14277-97-5
- IWP-L6
Catalog No.:BCC5101
CAS No.:1427782-89-5
- 4-Chlorophenylguanidine hydrochloride
Catalog No.:BCC2382
CAS No.:14279-91-5
- Silybin B
Catalog No.:BCN7898
CAS No.:142797-34-0
- 5,7-Dimethoxyluteolin
Catalog No.:BCN8167
CAS No.:90363-40-9
- DPN
Catalog No.:BCC7088
CAS No.:1428-67-7
13C CP (cross-polarization) MAS (magic angle spinning) NMR and GIAO-CHF calculations of buspirone analogues. Part 1. 3a,4,7,7a-Tetrahydro-2-[4-[4-(2-quinolinyl)-1-piperazinyl]butyl ]-4,7-ethane-1H-isoindole-1,3(2H)-dione hydrochloride and hydrobromide.[Pubmed:9875604]
Solid State Nucl Magn Reson. 1998 Nov;13(1-2):63-70.
13C CP (cross-polarization) MAS (magic angle spinning) solid state NMR spectra of buspirone analogue 3a,4,7,7a-tetrahydro-2-[4-[4-(2-quinolinyl)-1-piperazinyl]butyl]-4,7-eth ane-1H-isoindole-1,3(2H)-dione were recorded. In the spectra of hydrochloride and hydrobromide, two sets of signals appeared, in agreement with single crystal X-ray diffraction data indicating that in each of the salts two independent cations were present in the crystal unit. The largest shielding differences of 3.2-4.6 ppm between two sets of signals were found for quinoline aromatic carbons C3 and C2. Ab initio calculations of the carbon and nitrogen shielding constants were performed with the use of the GIAO-CHF method for structural fragments: N-butylsuccinimide, quinoline-(N-methyl) piperazine hydrochloride and hydrobromide. Linear correlations between theoretical and solid state results were obtained, thus enabling a reasonable assignment of carbon resonances of the conformations present in the solid state. Due to the fast dynamics in solution, the carbon chemical shifts corresponded to the averaged values of the forms present in the solid state.
Discovery of 1-[9-(4-chlorophenyl)-8-(2-chlorophenyl)-9H-purin-6-yl]-4-ethylaminopiperidine-4- carboxylic acid amide hydrochloride (CP-945,598), a novel, potent, and selective cannabinoid type 1 receptor antagonist.[Pubmed:19102698]
J Med Chem. 2009 Jan 22;52(2):234-7.
We report the structure-activity relationships, design, and synthesis of the novel cannabinoid type 1 (CB1) receptor antagonist 3a (CP-945,598). Compound 3a showed subnanomolar potency at human CB1 receptors in binding (Ki = 0.7 nM) and functional assays (Ki = 0.12 nM). In vivo, compound 3a reversed cannabinoid agonist-mediated responses, reduced food intake, and increased energy expenditure and fat oxidation in rodents.
N-(3,4-dimethoxyphenethyl)-4-(6,7-dimethoxy-3,4-dihydroisoquinolin-2[1H]-yl)-6,7- dimethoxyquinazolin-2-amine (CP-100,356) as a "chemical knock-out equivalent" to assess the impact of efflux transporters on oral drug absorption in the rat.[Pubmed:19373887]
J Pharm Sci. 2009 Dec;98(12):4914-27.
The utility of the diaminoquinazoline derivative CP-100,356 as an in vivo probe to selectively assess MDR1/BCRP-mediated drug efflux was examined in the rat. CP-100,356 was devoid of inhibition (IC(50) >50 microM) against major human P450 enzymes including P4503A4. In human MDR1-transfected MDCKII cells, CP-100,356 inhibited acetoxymethyl calcein (calcein-AM) uptake (IC(50) approximately 0.5 +/- 0.07 microM) and digoxin transport (IC(50) approximately 1.2 +/- 0.1 microM). Inhibition of prazosin transport (IC(50) approximately 1.5 +/- 0.3 microM) in human BCRP-transfected MDCKII cells by CP-100,356 confirmed the dual MDR1/BCRP inhibitory properties. CP-100,356 was a weak inhibitor of OATP1B1 (IC(50) approximately 66 +/- 1.1 microM) and was devoid of MRP2 inhibition (IC(50) >15 microM). In vivo inhibitory effects of CP-100,356 in rats were examined after coadministration with MDR1 substrate fexofenadine and dual MDR1/BCRP substrate prazosin. Coadministration with increasing doses of CP-100,356 resulted in dramatic increases in systemic exposure of fexofenadine (36- and 80-fold increase in C(max) and AUC at a CP-100,356 dose of 24 mg/kg). Significant differences in prazosin pharmacokinetics were also discernible in CP-100,356-pretreated rats as reflected from a 2.6-fold increase in AUC. Coadministration of CP-100,356 and P4503A substrate midazolam did not result in elevations in systemic exposure of midazolam in the rat. The in vivo methodology should have utility in drug discovery in selective and facile assessment of the role of MDR1 and BCRP efflux transporters in oral absorption of new drug candidates.
The equilibrium and kinetic drug binding properties of the mouse P-gp1a and P-gp1b P-glycoproteins are similar.[Pubmed:10555746]
Br J Cancer. 1999 Nov;81(5):783-9.
The gene encoding the multidrug resistance P-glycoprotein (P-gp) is duplicated in rodent species and the functional basis for this remains unresolved. Despite a high sequence similarity, the mouse P-gp1a and P-gp1b isoforms show distinct patterns of tissue distribution which suggest a specific role of the P-gp1b isoform in steroid transport. In the present study possible biochemical differences between the isoforms were directly investigated at the level of drug interaction. There was no detectable difference in the affinity or binding capacity of the two isoforms towards [3H]vinblastine at equilibrium. Similarly, the rate at which [3H]vinblastine associates with P-gp was indistinguishable between the two isoforms. Some modest differences were observed in the relative abilities of the multidrug-resistant (MDR) reversing agents CP100-356, nicardipine and verapamil to displace equilibrium [3H]vinblastine binding to P-gp1a and P-gp1b. The steroid hormone progesterone displayed a low affinity (Ki = 1.2 +/- 0.2 microM for P-gp1a and 3.5 +/- 0.5 microM for P-gp1b), suggesting an unlikely role as a physiological substrate. Thus the mouse isoforms do not appear to exhibit functional differences at the level of initial substrate interaction with protein.
P-glycoprotein and cytochrome P-450 3A inhibition: dissociation of inhibitory potencies.[Pubmed:10463589]
Cancer Res. 1999 Aug 15;59(16):3944-8.
Many P-glycoprotein (P-gp) inhibitors studied in vitro and in vivo are also known or suspected to be substrates and/or inhibitors of cytochrome P-450 3A (CYP3A). Such overlap raises the question of whether CYP3A inhibition is an intrinsic characteristic of P-gp inhibitors, a matter of concern in the development and rational use of such agents. Thus, the purpose of the present study was to determine whether the ability to inhibit P-gp and CYP3A is, in fact, linked and whether specific P-gp inhibitors with limited ability to inhibit CYP3A can be identified. Therefore, the potency of a series of 14 P-gp inhibitors was assessed by measuring their inhibition of the transepithelial flux across Caco-2 cells of digoxin, a prototypical P-gp substrate. CYP3A inhibition was determined from the impairment of nifedipine oxidation by human liver microsomes. Determination of the apparent Ki values for CYP3A inhibition and the IC50s for P-gp and CYP3A inhibition allowed comparison of the relative inhibitory potency of the compounds on the two proteins' function. The IC50s for P-gp inhibition ranged from 0.04 to 3.8 microM. All compounds inhibited CYP3A with apparent Ki values of between 0.3 and 76 microM and IC50s between 1.5 and 50 microM. However, no correlation was found between the extent of P-gp inhibition and CYP3A inhibition, and the ratio of the IC50 for CYP3A inhibition to the IC50 for P-gp inhibition varied from 1.1 to 125. These results demonstrate that, although many P-gp inhibitors are potent inhibitors of CYP3A, a varying degree of selectivity is present. The development and use of P-gp inhibitors with minimal or absent CYP3A inhibitory effects should decrease the impact of drug interactions on the therapeutic use of such compounds.