Just to expand upon Kelsee's post, here is the schedule with links/abstracts as well as who from RVX is attending according to Sarah (subject to change of course).

Nov. 2-4: Bio-Europe 2015, Munich, Germany. Resverlogix presents on Tuesday Nov 3rd. Don McCaffrey & Ken Lebioda are attending. Presentation will be prior to North American markets opening tomorrow.

Nov. 3-8: ASN Kidney Week, San Diego, CA. American Society for Nephrology conference. Ken Lebioda & Chris Halliday are attending. Dr. Kaymar Kalantar-Zadeh is presenting the following on Thursday Nov. 5th (full abstracts at end of message):

• Nov 5: The Epigenetic BET-Inhibitor RVX-208/Apabetalone Shows Favorable Effects on ALP and eGFR in Chronic Kidney Disease (CKD) Patients – A Post-Hoc Analysis of Phase 2 Clinical Trials
• Nov 5: Alkaline Phosphatase Lowering by Selective BET Inhibition, a Novel Mechanism for MACE Reduction in High Risk CVD, Diabetes and CKD Patients – A Post-Hoc Analysis of Phase 2b Studies with RVX-208

Nov. 5-7: CTAD 2015, Barcelona, Spain. Clinical Trials on Alzheimer's Disease conference. Ewelina Kulikowski is attending.

Nov. 5-9: Zenith is attending AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, Nov 5-9 2015 in Boston. Zenith presents the following on Sunday November 8th (full abstract at end of message):

• Nov 8: The clinical candidate ZEN-3694, a novel BET bromodomain inhibitor, is efficacious in the treatment of a variety of solid tumor and hematological malignancies, alone or in combination with several standard of care and targeted therapies

Nov. 7-11: AHA Conference 2015, Orlando, FL. American Heart Association Scientific Sessions. Norman Wong, Ken Lebioda , Mike Sweeney, Jan Johansson, & Chris Halliday are attending. Norman Wong from Resverlogix is presenting the following on Sunday November 8th (full abstract embargoed until day or presentation):

• Nov 8: RVX-208 a Selective Bromodomain and Extra-terminal BET Protein Inhibitor Acts on Several Pathways to Benefit Cardiovascular Risks

Here are the ASN Kidney week full abstracts.

Abstract: [TH-PO666] The Epigenetic BET-Inhibitor RVX-208/Apabetalone Shows Favorable Effects on ALP and eGFR in Chronic Kidney Disease (CKD) Patients – A Post-Hoc Analysis of Phase 2 Clinical Trials

Kamyar Kalantar-Zadeh, MD, PhD, MPH, FASN, Jan O. Johansson, MD, PhD, Michael Sweeney, MD, Kenneth E. Lebioda, Ewelina Kulikowski, PhD, Christopher Halliday, Norman Cw Wong, MD. Div of Nephrology & Hypertension, 1Univ of California Irvine School of Medicine, Irvine, CA; Research and Development, Resverlogix Corporation, Calgary, AB, Canada.

Background: The epigenetic BET inhibitor RVX-208 is a small molecule with anti-inflammatory and apolipoprotein A-I (apoA-I) enhancing effects. It exerts its' actions by inhibiting bromodomain extra-terminal proteins (BET) thus inhibiting acetylated lysine, present in histones, from binding to the same site. In this process chromatin structure is altered and activity of select genes inhibited. A subpopulation analysis from the double-blind placebo controlled phase 2b program in cardiovascular disease (CVD) identified 81 subjects with CKD based on eGFR < 60 ml/min/1.73m2. Methods: The effect of selective BET inhibition on key renal parameters in 81 CKD subjects (RVX-208 n=58/Placebo n=23) that were treated with either RVX-208 100mg/day or 150 mg b.i.d or matching placebo for 3 to 6 months were studied. A pooled analysis was performed to assess the changes from baseline for eGFR, ALP and creatinine at 3 and 6 months. Results: ALP changes for RVX-208 and placebo were -14.2% and -0.34% at 3 months (p<0.05 vs. placebo) and -13.9% vs. -6.28% (p<0.05 vs. placebo) at 6 months. Following 6 months of RVX-208 treatment, eGFR showed an increase of +3.4% (p=0.04 vs. baseline) in the RVX-208 group compared to a decrease of -5.9% in the placebo group. After 6 months treatment serum creatinine was decreased (-2.82%, p<0.10 vs. baseline) compared to increases in the placebo group of +3.0% and +4.85% at 3 and 6 months, respectively. No significant change in eGFR and serum creatinine were observed after 3 months RVX-208 treatment, albeit nominal numbers went in the normalization directions. Conclusions: Six months treatment with RVX-208, a selective BD2 selective BET-inhibitor significantly lowers serum ALP, and shows trends for eGFR and serum creatinine improvements. A phase 3 study BETonMACE is being planned in which these effects will be assessed in the prospective setting in diabetic CVD patients with or without CKD.

Abstract: [TH-PO609] Alkaline Phosphatase Lowering by Selective BET Inhibition, a Novel Mechanism for MACE Reduction in High Risk CVD, Diabetes and CKD Patients – A Post-Hoc Analysis of Phase 2b Studies with RVX-208

Kamyar Kalantar-Zadeh, MD, PhD, MPH, FASN, Jan O. Johansson, MD, PhD, Michael Sweeney, MD, Kenneth E. Lebioda, Ewelina Kulikowski, PhD, Christopher Halliday, Norman Cw Wong, MD. Div of Nephrology and Hypertension, 1Univ of California Irvine School of Medicine, Irvine, CA; Reseerch and Development, Resverlogix Corp, Calgary, AB, Canada.

Background: RVX-208 development is focused on reducing major adverse cardiovascular events (MACE) in high risk CVD, diabetes and CKD patients. RVX-208 is a first in class select BET inhibitor small molecule that interacts with the second ligand domain found in bromodomain and extra-terminal proteins (BET). It is characterized by reductions in alkaline phosphatase (ALP) and anti-inflammatory effects. Methods: In the SUSTAIN and ASSURE phase 2b clinical studies, high risk CVD patients were treated with 200 mg b.i.d RVX-208 or placebo for up to 26 weeks duration. Patients with a history of diabetes were analysed as a subgroup. Results: A significant reduction in MACE in all the RVX-208 treated patients (n=331) compared to placebo (n=168) was observed (p=0.02) as well as in those with diabetes (RVX-208 n=127/placebo n=65) (p<0.01). MACE included death, non-fatal myocardial infarct, and hospital admittance for cardiac reasons. In all patients (n=499), MACE compared to non-MACE patients had higher baseline ALP; 77.0 U/L vs. 72.0 U/L (p<0.05). Similar trends were observed in diabetes patients, 81.0 U/L vs. 75.5 U/L. RVX-208 treatment significantly lowered ALP vs. placebo in all patients (p<0.0001) and especially in those with diabetes (p<0.0001). In addition, in the RVX-208 treated group, patients who did not experience a MACE had greater reductions of ALP compared to those who experienced a MACE (-8.0 U/L vs. +3.0 U/L) (p<0.05). Conclusions: In phase 2b studies in high risk CVD and diabetes patients treated with RVX-208, a select BET-inhibitor, baseline ALP levels were significantly different between the MACE and non-MACE patients. Furthermore, RVX-208 significantly lowered serum ALP. A prospective phase 3 study currently planned, called BETonMACE, will need to further examine RVX-208's potential in reducing MACE in high risk CVD, diabetes and CKD patients.

Here is the Zenith AACR abstract:

Abstract Number:C86

Presentation Title:The clinical candidate ZEN-3694, a novel BET bromodomain inhibitor, is efficacious in the treatment of a variety of solid tumor and hematological malignancies, alone or in combination with several standard of care and targeted therapies

Author Block:Sarah Attwell, Eric Campeau, Ravi Jahagirdar, Olesya Kharenko, Karen Norek, Laura Tsujikawa, Cyrus Calosing, Reena Patel, Emily Gesner, Sanjay Lakhotia, Henrik Hansen. Zenith Epigenetics, Calgary, AB, Canada

Abstract Body:ZEN-3694 is an orally bioavailable small molecule discovered and developed from a BET bromodomain inhibitor discovery platform. In vitro, ZEN-3694 selectively binds to both bromodomains of the BET proteins, inhibiting the interaction of acetylated histone peptide with IC50 values in low nM range. ZEN-3694 inhibits proliferation of MV4-11 AML cells with an IC50 of 0.2 uM, and inhibits MYC mRNA expression with an IC50 of 0.16 uM.

ZEN-3694 has also demonstrated strong activity against many solid tumor and hematological cell lines with sub-uM IC50 values. In vitro synergy with Standard of Care (SOC) agents has been shown in a wide variety of malignancies including Breast, Prostate, Lung, Melanoma, AML, and DLBCL. Xenograft studies conducted with ZEN-3694 in AML, prostate and breast cancer models have demonstrated that it is efficacious at well-tolerated doses, modulating target gene expression and halting tumor growth in a dose-dependent manner.

In the AR positive VCAP prostate cancer cell line, ZEN-3694 inhibits proliferation synergistically with the AR antagonists enzalutamide and ARN-509. In an in vitro enzalutamide resistance model characterized by the up-regulation of the glucocorticoid receptor (GR), GR expression was inhibited by ZEN-3694 in a dose-dependent manner. Sensitivity to ZEN-3694 was unaltered, suggesting that it could be a valid therapeutic approach in patients developing resistance to AR antagonists through GR induction.

Robust PD modulation has been observed across multiple matrices for ZEN-3694 and will be explored further in the clinic. Promising target validation data, excellent pharmacological properties, and robust activity of ZEN-3694 across a variety of hematological malignancy and solid tumor settings support the clinical development of ZEN-3694 in various oncologic indications.