Modulators of glucocorticoid receptor, AP-1, and/or...

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Having -c- – wherein x is chalcogen – bonded directly to...

Reexamination Certificate

Rate now

  [ 0.00 ] – not rated yet Voters 0   Comments 0

Details

C514S367000, C514S254020, C514S353000, C514S236200, C514S236800, C514S255060, C514S256000, C514S398000, C514S377000, C514S404000, C514S314000, C514S622000, C514S352000, C514S342000, C514S361000, C514S254030, C544S133000, C544S134000, C544S131000, C544S329000, C544S336000, C544S367000, C544S369000, C546S233000, C546S221000, C546S309000, C546S270700, C548S195000, C548S163000, C548S139000, C548S140000, C548S332100, C548S233000, C548S372500, C564S174000

Reexamination Certificate

active

07968577

ABSTRACT:
Novel non-steroidal compounds are provided which are useful in treating diseases associated with modulation of the glucocorticoid receptor, AP-1, and/or NF-κB activity including inflammatory and immune diseases, obesity and diabetes having the structure of formula (I) an enantiomer, diastereomer, tautomer, solvate (e.g. a hydrate), or a pharmaceutically-acceptable salt, thereof, wherein: M is selected from alkyl, substituted alkyl, cycloalkyl, aryl, heterocyclo, and heteroaryl, provided that if M is alkyl then R6and R7taken together with the carbon atom to which they are both attached are selected from a group other than cycloalkyl; Q is selected from (i) hydrogen, C1-C4alkyl, and substituted C1-C4alkyl; or (ii) Q and R6are combined with the carbon atoms to which they are attached to form a 3- to 6-membered cycloalkyl; or (iii) Q and MaM are combined with the carbon atom(s) to which they are attached to form a 3- to 7-membered ring containing 1-2 heteroatoms which are independently selected from the group consisting of O, S, SO2, and N which ring may be optionally substituted with 0-2 R5groups or carbonyl; Z is selected from cycloalkyl, heterocyclo, aryl, or heteroaryl; and Ma, Za, R1, R2, R3, R4, R6, R7, and R22are as defined herein. Also provided are pharmaceutical compositions and methods of treating metabolic and inflammatory- or immune-associated diseases or disorders using said compounds.

REFERENCES:
patent: 2004/0082568 (2004-04-01), Yang
patent: 2005/0004164 (2005-01-01), Caggiano et al.
patent: 8-231516 (1996-09-01), None
patent: WO 03/059899 (2003-07-01), None
patent: WO 2004/005261 (2004-01-01), None
patent: WO 2005/003098 (2005-01-01), None
patent: WO2008/021926 (2008-02-01), None
patent: WO2008/057856 (2008-05-01), None
patent: WO2008/057859 (2008-05-01), None
patent: WO2008/057867 (2008-05-01), None
CAplus Registry entry for Registry No. 500534-63-4 (entered STN on Mar. 25, 2003).
Butke et al. J. Org. Chem. 1978, 43, 954-960.
Sheridan, J. Chem. Inf. Comput. Sci., vol. 42, 2002, 103-108.
Baldwin, Jr., A.S., “The transcription factor NF-κB and human disease”, The Journal of Clinical Investigation, vol. 107, No. 1, pp. 3-6 (2001).
Burke, J.R., “Targeting IκB kinase for the treatment of inflammatory and other disorders”, Current Opinion in Drug Discovery & Development, vol. 6, No. 5, pp. 720-728 (2003).
Caldenhoven, E. et al., “Negative Cross-Talk between ReIA and the Glucocorticoid Receptor: A Possible Mechanism for the Antiinflammatory Action of Glucocorticoids”, Molecular Endocrinology, vol. 9, No. 4, pp. 401-412 (1995).
Chakravarti, D. et al., “Role of CBP/P300 in nuclear receptor signalling”, Nature, vol. 383, pp. 99-103 (1996).
Diamond, M.I. et al., “Transcription Factor Interactions: Selectors of Positive or Negative Regulation from a Single DNA Element”, Science, vol. 249, pp. 1266-1272 (1990).
Firestein, G.S. et al., “Signal Transduction and Transcription Factors in Rheumatic Disease”, Arthritis & Rheumatism, vol. 42, No. 4, pp. 609-621 (1999).
Jonat, C. et al., “Antitumor Promotion and Antiinflammation: Down-Modulation of AP-1 (Fos/Jun) Activity by Glucocorticoid Hormone”, Cell, vol. 62, pp. 1189-1204 (1990).
Kamei, Y. et al., “A CBP Integrator Complex Mediates Transcriptional Activation and AP-1 Inhibition by Nuclear Receptors”, Cell, vol. 85, pp. 403-414 (1996).
Manning, A.M., et al., “Targeting JNK for Therapeutic Benefit: from Junk to Gold?”, Nature, vol. 2, pp. 554-565 (2003).
Miesfeld, R. et al., “Characterization of a steroid hormone receptor gene and mRNA in wild-type and mutant cells”, Nature, vol. 312, pp. 779-781 (1984).
Peltz, G., “Transcription factors in immune-mediated disease”, Current Opinion in Biotechnology, vol. 8, pp. 467-473 (1997).
Reichardt, H.M. et al., “DNA Binding of the Glucocorticoid Receptor is Not Essential for Survival”, Cell, vol. 93, pp. 531-541 (1998).
Reichardt, H.M. et al., “Repression of inflammatory responses in the absence of DNA binding by the glucocorticoid receptor”, The EMBO Journal, vol. 20, No. 24, pp. 7168-7173 (2001).
Weinberger, C. et al., “Domain structure of human glucocorticoid receptor and its relationship to the v-erb-Aoncogene product”, Nature, vol. 318, pp. 670-672 (1985).
Weinberger, C. et al., “Identification of Human Glucocorticoid Receptor Complementary DNA Clones by Epitope Selection”, Science, vol. 228, pp. 740-742 (1985).
Yang-Yen, H.-F. et al., “Transcriptional Interference between c-Jun and the Glucocorticoid Receptor: Mutual Inhibition of DNA Binding Due to Direct Protein-Protein Interaction”, Cell, vol. 62, pp. 1205-1215 (1990).

LandOfFree

Say what you really think

Search LandOfFree.com for the USA inventors and patents. Rate them and share your experience with other people.

Rating

Modulators of glucocorticoid receptor, AP-1, and/or... does not yet have a rating. At this time, there are no reviews or comments for this patent.

If you have personal experience with Modulators of glucocorticoid receptor, AP-1, and/or..., we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Modulators of glucocorticoid receptor, AP-1, and/or... will most certainly appreciate the feedback.

Rate now

     

Profile ID: LFUS-PAI-O-2627396

  Search
All data on this website is collected from public sources. Our data reflects the most accurate information available at the time of publication.