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Rec 15/2615 dihydrochloride

CAS# 173059-17-1

Rec 15/2615 dihydrochloride

Catalog No. BCC7628----Order now to get a substantial discount!

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Chemical structure

Rec 15/2615 dihydrochloride

3D structure

Chemical Properties of Rec 15/2615 dihydrochloride

Cas No. 173059-17-1 SDF Download SDF
PubChem ID 56972225 Appearance Powder
Formula C26H35Cl2N5O5 M.Wt 568.49
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO
Chemical Name 1-[4-(4-amino-6,7-dimethoxyquinazolin-2-yl)piperazin-1-yl]-2-(2-methoxy-6-propan-2-ylphenoxy)ethanone;dihydrochloride
SMILES CC(C)C1=C(C(=CC=C1)OC)OCC(=O)N2CCN(CC2)C3=NC4=CC(=C(C=C4C(=N3)N)OC)OC.Cl.Cl
Standard InChIKey XZGSTPYGKYGQLD-UHFFFAOYSA-N
Standard InChI InChI=1S/C26H33N5O5.2ClH/c1-16(2)17-7-6-8-20(33-3)24(17)36-15-23(32)30-9-11-31(12-10-30)26-28-19-14-22(35-5)21(34-4)13-18(19)25(27)29-26;;/h6-8,13-14,16H,9-12,15H2,1-5H3,(H2,27,28,29);2*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.

Biological Activity of Rec 15/2615 dihydrochloride

DescriptionSelective α1B-adrenoceptor antagonist (Ki values are 0.3, 1.9 and 2.6 nM at human α1B, α1A and α1D receptors respectively).

Rec 15/2615 dihydrochloride Dilution Calculator

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Rec 15/2615 dihydrochloride Molarity Calculator

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Preparing Stock Solutions of Rec 15/2615 dihydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.759 mL 8.7952 mL 17.5905 mL 35.1809 mL 43.9761 mL
5 mM 0.3518 mL 1.759 mL 3.5181 mL 7.0362 mL 8.7952 mL
10 mM 0.1759 mL 0.8795 mL 1.759 mL 3.5181 mL 4.3976 mL
50 mM 0.0352 mL 0.1759 mL 0.3518 mL 0.7036 mL 0.8795 mL
100 mM 0.0176 mL 0.088 mL 0.1759 mL 0.3518 mL 0.4398 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.

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References on Rec 15/2615 dihydrochloride

Alpha(1A)-adrenoceptors mediate contractions to phenylephrine in rabbit penile arteries.[Pubmed:17115072]

Br J Pharmacol. 2007 Jan;150(1):112-20.

BACKGROUND AND PURPOSE: Maintained penile erection depends on the absence of alpha-adrenoceptor (alpha-AR) activation and so can be facilitated by alpha-blockers. This study seeks the alpha(1)-AR subtypes involved in order to inform the pro-erectile consequences of subtype selective blockade. EXPERIMENTAL APPROACH: Wire myography was used with dorsal (nutritional supply) and cavernous (erectile inflow) penile arteries; standard alpha-AR-selective agonists and antagonists were employed to classify responses. KEY RESULTS: In both penile arteries noradrenaline (NA) and phenylephrine (PE, alpha(1)-AR agonist) caused concentration-dependent contractions. Sensitivity to NA was increased by NA uptake blockers, cocaine (3 microM) and corticosterone (30 microM). PE responses were antagonised by phentolamine (non-selective alpha-AR: dorsal pK(B) 8.00, cavernous 8.33), prazosin (non-subtype-selective alpha(1)-AR: dorsal 8.60, cavernous 8.41) and RS100329 (alpha(1A)-AR selective: dorsal 9.03, cavernous 8.80) but not by BMY7378 (alpha(1D)-AR selective: no effect at 1-100 nM) or Rec15/2615 (alpha(1B)-AR selective: no effect at 1-100 nM). Schild analysis was straightforward in cavernous artery, indicating that PE activates only alpha(1A)-AR. In dorsal artery Schild slopes were low, though alpha(1A)-AR was still indicated. Analysis using UK 14,304 and rauwolscine indicated an alpha(2)-AR component in dorsal artery that may account for low slopes to alpha(1)-AR antagonists. CONCLUSIONS AND IMPLICATIONS: Penile arteries have a predominant, functional alpha(1A)-AR population with little evidence of other alpha(1)-AR subtypes. Dorsal arteries (nutritional supply) also have alpha(2)-ARs. Thus, alpha-AR blockers with affinity for alpha(1A)-AR or alpha(2)-AR would potentially have pro-erectile properties; the combination of these perhaps being most effective. This should inform the design of drugs to assist/avoid penile erection.

Ligand design for alpha1 adrenoceptor subtype selective antagonists.[Pubmed:10968279]

Bioorg Med Chem. 2000 Jan;8(1):201-14.

Alpha1 adrenoceptors have three subtypes and drugs interacting selectively with these subtypes could be useful in the treatment of a variety of diseases. In order to gain an insight into the structural principles governing subtype selectivity, ligand based drug design (pharmacophore development) methods have been used to design a novel 1,2,3-thiadiazole ring D analogue of the aporphine system. Synthesis and testing of this compound as a ligand on cloned and expressed human alpha1 adrenoceptors is described. Low binding affinity was found, possibly due to an unfavourable electrostatic potential distribution. Pharmacophore models for antagonists at the three adrenoceptor sites (alpha1A, alpha1B, alpha1D) were generated from a number of different training sets and their value for the design of new selective antagonists discussed. The first preliminary antagonist pharmacophore model for the alpha1D adrenoceptor subtype is also reported.

Pharmacological characterization of the uroselective alpha-1 antagonist Rec 15/2739 (SB 216469): role of the alpha-1L adrenoceptor in tissue selectivity, part II.[Pubmed:9190864]

J Pharmacol Exp Ther. 1997 Jun;281(3):1284-93.

The aim of the present work was to investigate whether or not the uroselectivity of Rec 15/2739 and several other alpha-1 adrenoceptor (alpha1-AR) antagonists observed in the anesthetized dog could be related to selectivity of these compounds for a particular alpha-1 AR subtype. The binding affinity of the tested compounds for canine prostate alpha-1 ARs and their in vitro functional affinity for the alpha-1 ARs of rabbit urethra and prostate correlated with their functional affinity for the alpha-1L AR subtype, but not with the binding affinity for recombinant animal and human alpha-1a, alpha-1b and alpha-1d AR subtypes. Similar results were obtained when the in vivo potency on urethral pressure was correlated with the affinity for the alpha-1 AR subtypes; also in this case alpha-1L AR gave the best correlation. No correlation was obtained by considering the other alpha-1 AR subtypes. The in vivo hypotensive effects observed in dog after i.v. administration of the considered compounds correlated only with the binding affinity for the animal and human alpha-1d subtype. In conclusion, the results shown in the present paper indicate that the potencies of different alpha-1 antagonists against the contractions induced by norepinephrine on tissues of the lower urinary tract of rabbits and dogs are better correlated with their affinity for the putative alpha-1L subtype than for the alpha-1a subtype. Only the compounds showing selectivity for the alpha-1L subtype versus the alpha-1d subtype proved highly selective in vivo for the lower urinary tract versus the vascular tissues.

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