DR. ANDRZEJ T SLOMINSKI, M.D.
Medical Practice at Madison Ave, Memphis, TN

7253293, Aug 7, 2007

Jan 6, 2005

11/031844

Andrzej Slominski - Memphis TN, US
Robert Tuckey - Crawley, WA 6009, AU
Jordan Zjawiony - Oxford MS, US
D. Jeremy Stewart - Water Valley MS, US
Jacobo Wortsman - Springfield IL, US

C07C 401/00

552653

Provided herein are enzymatic methods of producing steroid compounds such as 7-dehydropregnenolone, hydroxy derivatives thereof and vitamin D2- and D3-like compounds and derivatives thereof. Also provided are the derivatives of the vitamin D3-like compounds so generated via the action of cytochrome P450scc enzyme on substrates 7-dehydrocholesterol, vitamin D2 or vitamin D3.

2007005, Mar 15, 2007

Jul 29, 2005

11/193801

Andrzej Slominski - Germantown TN, US
Alexander Pisarchik - Lauderdale MN, US

C12Q 1/68, G06F 19/00, C12P 19/34, C12M 1/34

435006000, 435091200, 435287200, 702020000, 977924000

The present invention provides a novel DNA microarray chip that can be used for simultaneous testing of transcriptional responses to cutaneous stressors in the context of neuro-endocrine-immune functions of the skin. The transcriptional responses to ultraviolet radiation in epidermal keratinocytes were tested using such microarray chip containing more than 700 neuro-endocrine-immune related genes. The gene expression pattern was non-random and time dependent; it included increased expression of genes involved in water and salt balance, prostaglandin synthesis, keratinocyte differentiation as well as genes coding for stress effectors, cytokines and metalloproteinases. In contrast, expression was decreased for genes coding for growth factors and their receptors, and for elements of extracellular matrix. This stochastic pattern suggests that transcriptional responses are coordinated and aimed at preservation of epidermal barrier function, prevention of early carcinogenic events and remodeling of extracellular matrix.

2007021, Sep 20, 2007

Feb 21, 2007

11/708832

Andrzej Slominski - Germantown TN, US
Trevor Sweatman - Memphis TN, US
Tobias Fischer - Lubeck, DE
Igor Semak - Minsk, BY

A61K 8/49

424059000

Melatonin, which can be produced in the skin, exerts a protective effect against damage induced by ultraviolet radiation (UVR). The present study investigated the effect of UVB, the most damaging component of UVR, on melatonin metabolism in HaCaT keratinocytes and in a cell-free system. Four metabolites were identified by HPLC and LC-MS: 6-hydroxymelatonin, AFMK, 2-hydroxymelatonin (the main intermediate between melatonin and AFMK) and 4-hydroxymelatonin. Concentrations of these photoproducts were directly proportional to UVR-dose and to melatonin substrate content, and their accumulation was time dependent. The UVR-dependent increase of AFMK and 2-hydroxymelatonin was also detected in keratinocytes, where it was accompanied by simultaneous consumption of intracellular melatonin. Of note, melatonin and its two major metabolites, 2-hydroxymelatonin and AFMK, were also detected in untreated keratinocytes, neither irradiated nor preincubated with melatonin. Thus, intracellular melatonin metabolism is enhanced under exposure to UVR. The additional biological activity of these individual melatonin metabolites increases the spectrum of potential actions of the recently identified cutaneous melatoninergic system.

2011011, May 19, 2011

Aug 30, 2010

12/807178

Andrzej Slominski - Memphis TN, US
Wei Li - Germantown TN, US
Blazej Zbytek - Decatur GA, US
Robert C. Tuckey - Nedlands, AU
Jordan K. Zjawiony - Oxford MS, US
Minh Ngoc Nguyen - Morley, AU
Zorica Janjetovic - Memphis TN, US
Michal A. Zmijewski - Gdansk, PL
Trevor W. Sweatman - Memphis TN, US
Duane D. Miller - Memphis TN, US
Jianjun Chen - Memphis TN, US
Arnold E. Postlethwaite - Eads TN, US

A61K 31/57, C07J 5/00, C12N 5/00, A61P 35/00, A61P 35/02, A61P 17/00, A61P 19/02, A61P 3/10, A61P 3/04, A61P 9/10, C12P 33/06

514182, 552592, 435375, 435 58

Provided herein are steroidal compounds that are androsta-5,7-dienes or a pregna-5,7-dienes and ultraviolet B (UVB) conversion products thereof which includes pharmaceutical compositions of the steroidal compounds as shown in Tables 1 and 2. Also provided is a method for producing hydroxylated metabolites of cholecalciferol or ergocalciferol via the P450scc (CYP11A1) or CYP27B1 enzyme systems where the hydroxylase has an activity to hydroxylate position C20 of a secosteroid or its 5,7-dieneal precursor and the hydroxylated metabolites so produced. In addition, a method for inhibiting proliferation of either a normally or abnormally proliferating cell by contacting the cell with any of the compounds described herein. A related method is provided of treating a condition associated with the proliferating cell such as a cancer, a skin disorder, a defect in cell differentiation, cosmetic, prophylaxsis, or healthy cell maintenance.

7071161, Jul 4, 2006

Sep 13, 2002

10/242822

Alexander Pisarchik - Cordova TN, US
Andrzej Slominski - Germantown TN, US

The University of Tennessee Research Corporation - Knoxville TN

C07K 14/72, A61K 38/16

514 12, 530350, 530306

The present invention identifies four new isoforms of human corticotropin releasing hormone receptor type 1 (CRH-R1e, 1f, 1g and 1h) and three new isoforms of mouse corticotropin releasing hormone receptor type 1 (mCRH-R1c, 1e and 1f). The data indicate that polymorphism of CRH-R1 expression is related to anatomic location, skin physiological or pathologic status, specific cell type, external stress (UV), and that cAMP dependent pathways and TPA may regulate CRH-R1.

2006014, Jun 29, 2006

Feb 21, 2006

11/358841

Alexander Pisarchik - Cordova TN, US
Andrzej Slominski - Germantown TN, US

C12P 21/06, C07H 21/04, C07K 14/72, C07K 16/28

435069100, 435320100, 435325000, 530350000, 530388220, 536023500

The present invention identifies four new isoforms of human corticotropin releasing hormone receptor type 1 (CRH-R1e, 1f, 1g and 1h) and three new isoforms of mouse corticotropin releasing hormone receptor type 1 (mCRH-R1c, 1e and 1f). The data indicate that polymorphism of CRH-R1 expression is related to anatomic location, skin physiological or pathologic status, specific cell type, external stress (UV), and that cAMP dependent pathways and TPA may regulate CRH-R1.