Patent US8. 66. 92. Phenazine derivatives and uses thereof as potassium channel modulators. The present application is a continuation of International Application No. PCTUS2. 00. 80. WO2. Sep. 2. 2, 2. 00. U. S. Provisional Application number 6. Sep. 2. 1, 2. 00. U. S. Provisional Application number 6. Aug. 2. 2, 2. 00. SEQUENCE LISTINGThe instant application contains a Sequence Listing which has been submitted via EFS Web and is hereby incorporated by reference in its entirety. Said ASCII copy, created on May 6, 2. A abbreviation abbr bdomenaabdominal bdominala1. Brownfreq worrisome worry worryworryin worrying worse worsened worsens worship worshiped worshipful worshiping worshipped worshippers worshipping worst worstmarked. The word enamine is derived from the affix en used as the suffix of alkene, and the root amine. This can be compared with enol, which is a functional group. BACKGROUND OF THE INVENTIONAutoimmune disease occurs when a component of the immune system causes damage to the body Harvey Champe. Immunology. 2. 00. Williams Wilkins, Philadelphia, Pa. A number of autoimmune diseases exist which cause physical damage and greatly impact the quality of life of the sufferer. Functional uses flavor and fragrance agents. Has a floral type odor and an floral type flavor. Several autoimmune diseases such as lupus may result in death if left unchecked. Current therapies for treatment of autoimmune disease have produced varying degrees of efficacy and in many cases unacceptable adverse event profiles. A clear unmet need exists for better treatments of autoimmune diseases. Iodination Of Acetone Activation' title='Iodination Of Acetone Activation' />Better therapeutics could result from treating the underlying pathologies of autoimmune diseases. The etiology of the various diseases is complex and differs from disease to disease. However, a number of autoimmune diseases can be partly attributed to the pathological actions of T cells that either release substances which damage tissue or which activate other immune cells which cause damage. Psoriasis Sabet et al. Experimental Dermatology. Cope et al. Clin Exp Rheumatol. Suppl 4. 6 5. 4 1, multiple sclerosis MS Winquist et al. Biochemical Pharmacology. I diabetes Mallone et al. Curr Diab Rep. 2. T cells are believed to play a contributory role to disease pathology. Several therapeutics including alefacept Lev Tov et al., Rev Recent Clin. Trials. 2. 00. 6. FK 5. 06 and cyclosporine exert therapeutic actions by suppressing the activity of T cells. The use of such T cells suppressive drugs has been greatly limited to due to the global immunosuppressive nature of the agents. A need exists for a therapy which has the ability to suppress the pathological actions of T cells without causing general immunosupression which leads to an increased risk of infection. One potential strategy for selective T cell suppression is to target activated effector memory T cells while leaving central nave T cells untouched. One such strategy would be to target a component of T cells which is upregulated in pathological effector memory cells and which is also critical for the activation of the T cell. The potassium channel Kv. Chandy et al. TIPS. Kv. 1. 3 is a critical component of the Calcium Release Activated Channel CRAC signaling pathway. In a simplified summary, upon activation of the CD3T cell receptor complex e. C is activated which in turn causes release of calcium from the endoplasmic reticulum. The intracellular stores of calcium activate the CRAC channel which causes the influx of calcium and subsequent downstream signaling to the critical components of T cell activation including calcineurin and nuclear factor of activated T cells NFAT. In order for the continued influx of calcium through CRAC to continue, efflux of positively charged potassium is necessary to maintain the membrane potential. This potassium efflux can occur through either Kv. IKCa. 1 channel. The specific role of T cells expressing high levels of Kv. T cell mediated. In MS patients, the number of Kv. T cells and a specific Kv. T cells Wulff et al. J. Clin. Invest. 2. Furthermore, a Kv. EAE in rats, which is considered a standard animal model for MS Beeton et al. Proc. Natl. Acad. Sci. USA. 2. 00. 1. Likewise, Kv. 1. 3 was shown to be upregulated in T cells isolated from the synovial fluid of rheumatoid arthritis patients and a Kv. Mouth Of The South Transparency Zip here. Beeton et al. Proc. Natl. Acad. Sci. USA. Beeton et al. further showed that a Kv. Kv. 1. 3 was also upregulated in islet reactive T cells isolated from Type I Diabetes patients and Kv. Crack Outlook Express 6. T cells Beeton et al. Proc. Nall. Acad. Sci. USA. 2. 00. 6. Manuale Trucco M40s. Beeton et al. also showed that a Kv. Azam et al. showed that Kv. Azam et al. J. Investigative Dermatology. Kv. 1. 3 has also been suggested as a target for type 2 diabeties, as Kv. Kv. 1. 3 results in translocation of the glucose transporter GLUT4 to the plasma membrane Xu et al. Proc. Natl. Acad. Sci. USA. 2. 00. 4. The effects of Kv. GLUT4 transport Li et al. Am J Physiol Cell Physiol. C3. 45 C3. 51. A variant in the promoter of the Kv. Tschritter et al. The Journal of Clinical Endocrinology Metabolism. Accordingly, Kv. 1. Kv. 1. 3 which has an adverse event and pharmacokinetic profile such that the inhibitor is therapeutically viable. SUMMARY OF THE INVENTIONIt has now been found that compounds of this invention are effective as modulators of Kv. Such compounds have the general formula I or a pharmaceutically acceptable salt thereof, wherein each of W, Q, R2, R3, R4, R5, m, and n is as defined herein. Compounds of the present invention and pharmaceutically acceptable compositions thereof, are useful for treating a variety of diseases, disorders or conditions, mediated by Kv. T cell activation such as activation of effector memory T cells. Such diseases, disorders, or conditions include those described herein. Compounds provided by this invention are also useful for the study of Kv. Kv. 1. 3, and the comparative evaluation of new Kv. BRIEF DESCRIPTION OF THE DRAWINGSFIG. Clofazimine inhibits IL 2 production and NFAT activation in Jurkat T cells. A Clofazimine inhibits IL 2 proximal promoter driven luciferase stimulated by PMAionomycin in Jurkat T cells n6. The IC5. 0 for reporter assay is 2. M. B Clofazimine inhibits IL 2 production in PMAthapsigargin stimulated Jurkat T cells IC5. M and human mixed lymphocyte reaction MLR IC5. M n6 each. C Clofazimine inhibits NFAT pathway in Jurkat T cells. The IC5. 0s of clofazimine in the IL 2, NFAT, NF B luciferase reporter assays are 5. M, 1. 133. 0 n. M and 2. M, respectively n6 each. Both reporters were stimulated with PMAionomycin. D Clofazimine significantly enhances AP 1 luciferase reporter at high concentrations 1 M, n6. The reporter was also stimulated by PMAionomycin. E Clofazimine inhibits dephosphorylation of endogenous NFATc. NFATc. 2 and tubulin were detected by Western blot using specific antibodies. FIG. 2. Clofazimine interferes with calcium influx in Jurkat T cells. A Calcium influx was inhibited by clofazimine in a heterogeneous fashion. Clofazimine was added 5 minutes before stimulation with 1 M TG. Representative images were taken 3. M calcium was added. The color gradient represents fura 2 3. B Effects of clofazimine on store depletion induced calcium influx. Typically the cells can be divided into 2 groups, the responsive red and none responsive pink populations. Each curve represents average signal of 2. A The results were reproduced 1. C Effect of clofazimine on calcium oscillation in Jurkat T cells representative of 5. The oscillation was stimulated by 1. M TG. D Clofazimine elongated oscillation period in more than 8. Jurkat T cells Results represented 3 experiments, at least 8. FIG. 3. Clofazimine inhibits the Kv. A Averaged time course of Kv. Jurkat T cells in the absence and the presence of clofazimine CLF or margatoxin MGX. Various concentrations of CLF n5 each or 1.