Here are the events leading up to the Resverlogix Annual General Meeting on September 30th.

August 29 - September 2: European Society of Cardiology (ESC) Congress 2015, London, England. Norman Wong is listed as having an August 30th poster presentation at 8:30 AM (London) in the poster session entitled: Lipids in atherosclerosis. The poster is titled: "RVX-208, an orally active BET inhibitor, lowers CVD risk by activities beyond raising ApoA-1/HDL." No abstract is available at this time, but very likely similar content to what will be presented at EASD in mid-September (see below).

September 8-10: 17th Annual Global Investment Conference Rodman & Renshaw 2015 in New York. Resverlogix will present on September 10.

September 14-18: European Association for the Study of Diabetes in Stockholm, Sweden. Resverlogix is presenting an oral presentation on Friday September 18th at ~ 12PM (Sweden) entitled "RVX-208 acts via an epigenetic mechanism to lower Major Adverse Cardiovascular Events (MACE) in patients with atherosclerosis and especially in those with diabetes mellitus." The abstract for this is pasted below:

"RVX-208 acts via an epigenetic mechanism to lower Major Adverse Cardiovascular Events (MACE) in patients with atherosclerosis and especially in those with diabetes mellitus.

N.C.W. Wong1, E. Kulikowski1, L. Tsujikawa1, D. Gilham1, S. Wasiak1, C. Halliday1, K. Lebioda1, J.O. Johansson2, M. Sweeney2; 1Clinical Development, Resverlogix Corporation, Calgary, Canada, 2Clinical Development, Resverlogix Corporation, San Francisco, USA.

Background and aims: RVX-208 binds selectively to the second ligand domain of Bromodomain and Extra-Terminal (BET) proteins and inhibits their activity. Each BET protein has two bromodomains that bind acetylated lysines in histones. When a BET protein binds ligand, it recruits transcriptional machinery to DNA and thereby modifies gene activity. Analysis of pooled data from two phase 2b trials; SUSTAIN and ASSURE revealed a 55% relative risk reduction (RRR) of MACE in RVX-208 treated patients (n=331) vs. placebo (n=168). But in those with diabetes mellitus (DM) RVX-208 treatment lead to a 77% RRR of MACE vs. placebo. RVX-208 increased production of ApoA-I yielding more high-density lipoprotein (HDL) particles. While these effects should lower MACE, the magnitude was more than expected, prompting studies to identify properties of RVX-208 beyond its effects on ApoA-I/HDL.

Materials and methods: Plasma biomarkers from SUSTAIN and ASSURE trials were analyzed. Microarray data from RVX-208 treated primary human hepatocytes (PHH) or human whole blood (HWB) were used to identify differentially expressed genes, and guide measurements of specific proteins in clinical samples to confirm key findings.

Results: Biomarkers from the trials showed significant increases (p<0.05, unless specified) between RVX-208 vs. placebo in: HDL-c (+3mg/dL), ApoA-I (+7.5mg/dL), large HDL (+0.7umol/L), HDL size (+0.1nm), and total HDL particles (+1.8umol/L, p<0.07). Glucose in all patients (n=499) or in those with DM (n=192) given RVX-208 or placebo was unchanged vs baseline. In patients with DM (n=119) and low HDL (<40mg/dL), RVX-208 reduced glucose by -0.3 mmol/L but in placebo it increased +0.9 mmol/L. These modest changes do not predict the MACE reductions. Thus microarrays were used to survey PHH and HWB exposed to RVX-208. In PHH, RVX-208 decreased expression of genes in pathways for cholesterol & fatty acid synthesis, innate immunity and glucose processing. Most profound were effects on complement and coagulation pathways, where RVX-208 downregulated expression of 19/26 and 20/33 genes respectively. These data were confirmed by RT-PCR of key mRNAs. Furthermore, specific complement and coagulation proteins were found to be decreased in plasma from the trials (range 7-12% vs. baseline). Microarrays from HWB exposed ex-vivo to RVX-208 identified pathways with known roles in atherogenesis including: pro-inflammatory signaling, cell-cell interactions and extracellular matrix organization. RVX-208 significantly downregulated several pro-atherogenic genes (43/56) but upregulated anti-atherogenic genes (9/17), that control monocyte recruitment, migration and activation, macrophage function, inflammatory signaling and plaque stability to suggest an overall antiatherosclerotic benefit.

Conclusion: RVX-208 treatment is associated with marked MACE reductions in SUSTAIN and ASSURE patients and especially in those with DM. RVX-208 modifies cellular epigenetics to impact multiple biological processes that underlie CVD. Combined effects of RVX-208 on reverse cholesterol transport, vascular inflammation, innate immunity, atherosclerosis and thrombosis may explain its efficacy in reducing MACE.

Clinical Trial Registration Number: NCT01423188, NCT01067820"

The portion of the abstract regarding the human hepatocyte microarrays sounds similar between the ACC2015 and EASD2015 abstracts. But the language on the human whole blood (HWB) is new for EASD. Previously in the ACC2015 abstract, they indicated that "The microarray studies were performed using primary human liver cells exposed to RVX-208. This treatment demonstrated significant changes in cellular pathways or networks characterized by: an attenuation in inflammation, coagulation, complement and cholesterol synthesis." Now in the newer EASD abstract, it appears that they are looking at both primary hepatoctyes AND human whole blood treated with RVX-208 and as you can read in the abstract they have highlighted many more biological pathways that are beneficially modulated by RVX-208.

September 26: GCFF (Global Chinese Financial Forum) in Toronto. Don McCaffrey is giving the keynote speech (40 minute time slot starting at 9:30 AM) in the "Trend of Life Science Section". This is the first talk fo the morning for this one day event.

That's all that they list on their events page for now.

Best regards,

BDAZ