Full Press Release Details
O R P O R A T E P A R T I C I P A N T S
Senior Manager, Client Success, LifeSci Events
MD, SCD HC, Founder, President and Chief Executive Officer, Sellas Life Sciences
MD, Senior Vice President, Clinical Development, Sellas Life Sciences
MD, Professor, Department of Leukemia, University of Texas MD Anderson Cancer Center
MD, Associate Professor of Medicine, Chief of Leukemia Research, and Associate Chief of Research, Division of Hematology, UNC
Lineberger Comprehensive Cancer Center
Assistant Professor of Medicine and Associate Director of Bone Marrow Transplant Program, University of Alabama at Birmingham
O'Neil Comprehensive Cancer Center / Lead Investigator, Phase 3 REGAL Trial
Senior Vice President, Chief Commercial Officer, Sellas Life Sciences
O N F E R E N C E C A L L P A R T I C I P A N T S
Alliance Global Partners
R E S E N T A T I O N
attendees are in a listen-only mode. A question-and-answer session will follow the formal presentations. As a reminder, this call is
being recorded and a replay will be made available on the Sellas website following the conclusion of the event.
to turn the call over to your host, Dr. Angelos Stergiou, Founder, President and Chief Executive Officer of Sellas Life Sciences Group.
Please go ahead, Angelos.
morning everyone. Welcome to Sellas' GFH009 expert panel call.
you for your participation and support in joining us today. We're very excited to take this time to focus on some important
developments regarding the GFH009 program, particularly around the upcoming Phase 2a relapsed/refractory AML study, and very pleased
with FDA's comments and input to our trial design.
ViaVid has made considerable
efforts to provide an accurate transcription. There may be material errors, omissions, or inaccuracies in the reporting of the substance
of the conference call. This transcript is being made available for information purposes only. 1-888-562-0262 1-604-929-1352 www.viavid.com
to also be joined by Drs. Kadia, Zeidner and Jamy, as well as our Senior Vice President of Clinical Development, Dr. Dragan Cicic, and
our Senior Vice President, Chief Commercial Officer, Robert Francomano.
both of our assets, GPS and GFH009 have the potential to change the face of treatment for leukemia as well as other tumor types, but
today's focus is on relapsed/refractory acute myeloid leukemia with our highly selective CDK9 inhibitor GFH009.
at Sellas is to prolong patients' lives and to develop and deliver innovative treatments for patients battling cancer. With GPS, our
lead program in the Phase 3 REGAL study in AML, and our GFH009 programs, we now have two solid clinical assets with multiple shots on
goal to develop and potentially commercialize cancer drugs that can make a difference in patients' lives.
over to our KOLs, allow me to remind you why we brought in GFH009.
GFH009 is complementary
to GPS. This new drug candidate affords us the potential to expand further into the AML space to cover not only the maintenance phase,
which is the indication for GPS, but now also active disease in AML. Leveraging our vast experience in AML, GFH009 will allow us to expand
our clinical footprint into additional indications.
GPS in AML, in the third quarter of this year the IDMC will meet and provide feedback around the Phase 3 REGAL AML study in patients
in CR2. We expect our interim analysis by the end of this year or early next, but again, we should get further guidance by the IDMC in
GFH009, we completed the Phase 1 AML portion of the study and expect to open the relapsed/refractory AML Phase 2a study within June,
with ongoing data readouts and top line data by the end of this year. We also expect the Phase 1 top line lymphoma data within Q3 and
additional data readouts in lymphoma and potentially other indications on a rolling basis through studies being conducted by GenFleet.
Please remember that GenFleet has retained the rights to develop and commercialize GFH009 in Greater China, while we have the rights
to Rest of World. GenFleet is planning to focus mainly on lymphoma, while we focus on AML, and we each have rights to all of the data
coming out of the studies for our respective territories.
Venetoclax in combination
with hypomethylating agents is a staple of AML treatment across all patient categories, especially in older patients, which is the vast
majority of AML patients, preclinically as well as the Phase 1 patient who was relapsed refractory to aza/ven and went into remission
after our GFH009 monotherapy, we have seen that GFH009 exhibits a strong synergy with venetoclax and we believe that it may have the
potential to both improve response to venetoclax or to possibly even convert complete resistance to venetoclax into a strong response.
If we confirm this synergy in our Phase 2a study, this trait of GFH009 could profoundly change the standard of care in AML. Again, we're
investigating GFH009 to treat active disease and potentially get patients into a CR, and then GPS may be used in the maintenance phase
to keep patients in remission.
AML, lymphomas and soft tissue sarcomas, a significant proportion of almost all major cancer indications turns out to be transcription
addicted. It's the types of cancers GFH009 could be effective in, including breast cancer, osteosarcoma, endometrial cancer, lung cancer,
prostate cancer, melanoma and ovarian cancer. With established biomarkers, we envision a huge potential for use across broad swaths of
cancers with potentially hundreds of thousands of patients. We're starting with AML, the indication we know best, which could become
a true game changer, not only for AML, but for Sellas in general.
considerable efforts to provide an accurate transcription. There may be material errors, omissions, or inaccuracies in the reporting
of the substance of the conference call. This transcript is being made available for information purposes only. 1-888-562-0262 1-604-929-1352
like to turn it over to Dr. Dragan Cicic, who will provide a brief overview of the AML data to date with our GFH009 drug, as well as
the rationale behind and design of our Phase 2a AML study. We will then introduce our KOLs. Dragan?
I will provide a brief overview of our drug's mechanism of action, Phase 1 trial results and the upcoming Phase 2 trial design.
Let me start with the introduction to the mechanism of action.
selective CDK9 inhibitor. The main role of CDK9 is to enable transcription elongation of the RNA, resulting in rapid production of key
proteins that, among other roles, drive the vision of cancer cells and protect them from programmed cancer cell death. The biggest impact
of inhibiting CDK9 is therefore on short-lived cancer-enabling proteins, MYC and MCL1. Because these proteins are major cancer drivers,
cancers that rely on them we have poor prognosis and CDK inhibitors have potential to address specifically cancers with currently poor
outcomes like acute myeloid leukemia resistance to the standard azacitidine/venetoclax treatment, as Angelos mentioned. However, because
of the important roles kinases in general play in every cell, it is crucial to ensure that other kinases are not inhibited along with
CDK9. GFH009, as you can see on the slide at the bottom panel, has a very high selectivity compared to other drug candidates in the same
1 trial in relapsed and refractory AML and lymphoma, that selectivity allowed us to administer much higher doses of GFH009 without dose
limiting toxicities, two to four times higher than other CDK inhibitors in development, thus increasing the potential for efficacy without
any dose-limiting toxicities. To our knowledge, GFH009 is the only CDK9 inhibitor in development that as a single agent had a complete
response in relapsed/refractory AML. In addition to an MRD-negative complete response lasting more than six months as of now, we have
observed dose-dependent leukemia cell-killing activity at all dose levels studied, confirming GFH009's high therapeutic index, which
in turn allows for a high combinatorial potential.
Phase 2 trial is designed. This will be the first trial in AML, that I know of, that combines two antiapoptotic agents, a BCL2 inhibitor
and an indirect MCL1 inhibitor, and a proapoptotic agent, azacitidine. Furthermore, the trial is designed to directly assess the efficacy
of our antiapoptotic drug GFH009 because all patients enrolled will be the patients in whom a combination of venetoclax with proapoptotic
agents had already failed, and we will be investigating the restoration of efficacy of venetoclax combinations by adding GFH009.
will be a single-arm open-label multicenter trial conducted in the U.S. We will enroll up to 20 patients, all of whom will receive standard
doses of venetoclax and azacitidine, to which they are unresponsive, with the crucial addition of GFH009. GFH009 will be administered
at two dose levels, at the recommended Phase 2 dose level and one dose level below, namely 60 milligrams and 45 milligrams, to be administered
once a week and there will be 10 patients per dose level. Treatment will continue for as long as there are no dose-limiting toxicities
and no progression of disease. Bone marrow will be assessed after the first two infusions of GFH009, at Day 14 and then again at Day
28. Thereafter, bone marrow assessments will be every month, that is every 28 days.
for this trial will be composite complete response rate-CRC-duration of response and safety of the combination. Because of
the designated primary endpoints and frequency of assessments, we will have a very quick early readout on both efficacy and safety of
hand it over back to Angelos.
considerable efforts to provide an accurate transcription. There may be material errors, omissions, or inaccuracies in the reporting
of the substance of the conference call. This transcript is being made available for information purposes only. 1-888-562-0262 1-604-929-1352
to introduce our KOLs and ask them to provide a brief overview of their research interest and relevance around our GFH009 asset before
we start our fire chat discussion.
Dr. Kadia. Dr. Kadia is a professor in the Department of Leukemia at the University of Texas MD Anderson Cancer Center in Houston, Texas.
He serves as a co-leader of the sections of AML and Developmental Therapeutics and is the Associate Program Director of the Leukemia
Fellowship Program. He's actively involved in clinical and translational research for the treatment of patients with leukemia, and he
has authored over 375 peer-reviewed articles, numerous abstracts, and has been invited nationally and internationally for presentation
of his research. Dr. Kadia?
Good morning everyone.
As Angelos mentioned, my name is Tapan Kadia. I'm currently a professor in the Department of Leukemia. My focus for several years now