77508-59-9

Upstream product

• 39246-30-5 methyl 1,2,3,4-tetrahydronaphthalene-2-carboxylate 
• 6947-15-5 1,2,3,4-tetrahydro-2-naphthalene methanol 
• 53440-12-3 1,2,3,4-tetrahydro-2-naphthoic acid 

Relevant academic research and scientific papers

Use of alpha-1C specific compounds to treat benign prostatic hyperplasia

PCT No. PCT/US93/10950 Sec. 371 Date Apr. 1, 1997 Sec. 102(e) Date Apr. 1, 1997 PCT Filed Nov. 12, 1993 PCT Pub. No. WO94/10989 PCT Pub. Date May 26, 1994A method of treating benign prostatic hyperplasia in a subject which comprises administering to the subject a therapeutically effective amount of a compound which binds to a human alpha 1C adrenergic receptor with a binding affinity greater than ten-fold higher than the binding affinity with which the compound binds to a human alpha 1A adrenergic receptor, a human alpha 1B adrenergic receptor, and a human histamine H1 receptor, and, binds to a human alpha 2 adrenergic receptor with a binding affinity which is greater than ten-fold lower than the binding affinity with which the compound binds to such alpha 1C adrenergic receptor. Compounds meeting these criteria are provided.

ALPHA1C SPECIFIC COMPOUNDS TO TREAT BENIGN PROSTATIC HYPERPLASIA

This invention provides a method of treating benign prostatic hyperplasia in a subject which comprises administering to the subject a therapeutically effective amount of an α 1C antagonist which (a) binds to a human α 1C adrenergic receptor with a binding affinity greater than 100-fold higher than the binding affinity with which the α 1C antagonist binds to a human α 1A adrenergic receptor, a human α 1B adrenergic receptor, and a human histamine H 1 receptor; and (b) binds to a human α 2 adrenergic receptor with a binding affinity which is greater than 100-fold lower than the binding affinity with which the α 1C antagonist binds to such α 1C adrenergic receptor.The invention further provides a method of inhibiting contraction of a prostate tissue which comprises contacting the prostate tissue with an effective contraction-inhibiting amount of an α 1C antagonist which (a) binds to a human α 1C adrenergic receptor with a binding affinity greater than 100-fold higher than the binding affinity with which the α 1C antagonist binds to a human α 1A adrenergic receptor, a human α 1B adrenergic receptor, and a human histamine H 1 receptor; and (b) binds to a human α 2 adrenergic receptor with a binding affinity which is greater than 100-fold lower than the binding affinity with which the α 1C antagonist binds to such α 1C adrenergic receptor.

Aromatic amine derivatives

This invention relates to novel aromatic amine compounds having the structure: STR1 where each W, Z1 and Z2 is independently H, C1 -C6 alkyl, C1 -C6 alkoxy, OH, F, Cl, Br, I, NO2, CN, SO2 NHR3, NR42, CONR32, COR5 ; where each R1 and R2 is independently H, C1 -C6 straight or branched chain alkyl or phenyl; where each X and Y is independently CH2, NR4, S, S=O, SO2 ; where n is 0, 1 or 2; where each p and q is independently 1 or 2; where R3 is H, C1 -C6 straight or branched chain alkyl or phenyl; where R4 is H, C1 -C6 straight or branched chain alkyl or COR3 ; and where R5 is H, C1 -C6 straight or branched chain alkyl or phenyl, C1 -C6 straight or branched chain alkoxy or OH. In addition the invention includes using such compounds for the treatment of benign prostatic hyperplasia, lowering intraocular pressure and inhibiting cholesterol synthesis.

USE OF ALPHA-1C SPECIFIC COMPOUNDS TO TREAT BENIGN PROSTATIC HYPERPLASIA

The subject invention provides a method of treating benign prostatic hyperplasia in a subject which comprises administering to the subject a therapeutically effective amount of a compound which binds to a human . alpha. 1C adrenergic receptor with a binding affinity greater than ten-fold higher than the binding affinity with which the compound binds to a human α 1A adrenergic receptor, a human α 1B adrenergic receptor, a human histamine H 1 receptor and α 2 adrenergic receptor. The subject invention also provides a method of inhibiting contraction of prostate tissue which comprises contacting the prostate tissue with an effective contraction-inhibiting amount of such compound.

Use of α1C specific compounds to treat benign prostatic hyperlasia

A method of treating benign prostatic hyperplasia in a subject which comprises administering to the subject a therapeutically effective amount of a compound which binds to a human α1C adrenergic receptor with a binding affinity greater than ten-fold higher than the binding affinity with which the compound binds to a human α1A adrenergic receptor, a human α1B adrenergic receptor, and a human histamine H1 receptor, and, binds to a human α2 adrenergic receptor with a binding affinity which is greater than ten-fold lower than the binding affinity with which the compound binds to such α1C adrenergic receptor. Compounds meeting these criteria are provided.

The Stereochemistry of Ring Closure of Some Monosubstituted o-(But-3-enyl)phenyl Radicals

The rates and diastereoselectivity of cyclization of o-(but-3-enyl)phenyl radicals bearing substituents on the 1- or 2-position of the side chain have been examined. 1-Substituted radicals afford only 1,5-cyclization products, but 2-substituted radicals a

ARALKOXY AND ARYLOXYALKOXY KOJIC ACID DERIVATIVES

This invention relates to substituted aralkoxy and aryloxyalkoxy kojic acid derivatives, which are useful as leukotriene D. sub.4 (LTD 4) inhibitors and therefore useful in the treatment of allergies, inflammatory conditions, and coronary vasoconstriction.

Silanes in Organic Synthesis. 10. Cleavage Reactions of Silylcyclopropanes with Titanium Tetrachloride and Hydrogen Chloride

Seven trimethylsilyl-substituted cyclopropanes, both mono- and bicyclic, were treated with titanium tetrachloride and anhydrous hydrogen chloride to determine the regioselectivity and stereoselectivity of electrophilic attack on their strained three-membered ring.Whereas cleavage of exo-6-(trimethylsilyl)bicyclohexane with TiCl4 occurs predominantly at the zero bridge, the principal product obtained from treatment with HCl is the result of peripheral bond scission.In the case of exo-7-(trimethylsilyl)bicycloheptane, addition to an edge bond occurs regiospecifically with both reagents.Substrates 11 and 12 were examined to assess the importance of carbonium ion intervention.Structural isomerizations mediated by such intermediates were observed with both silylcyclopropanes.For 1-(trimethylsilyl)bicycloheptane and 1-(trimethylsilyl)-1-pentylcyclopropane, the altered position of the silicon substituent was seen to have a major effect on the course of ring opening.Although the present data allow some analogies to be drawn with vinylsilanes, it is clear that silylcyclopropanes have a broader range of reaction pathways available to them than do their olefinic counterparts.