On January 8, 2020 VBL Therapeutics (Nasdaq: VBLT) reported the publication of clinical data from the Phase 2 and Phase 3 studies of VB-111 (ofranergene obadenovec) in recurrent glioblastoma (rGBM) in two manuscripts published in the peer-reviewed journal Neuro-Oncology, the official journal of the Society for Neuro-Oncology (Press release, VBL Therapeutics, JAN 8, 2020, View Source [SID1234552857]).

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In the Phase 2 study, patients with rGBM who were primed with VB-111 monotherapy that was continued after progression with the addition of bevacizumab (Avastin) showed significant survival (414 vs 223 days; HR 0.48; p=0.043) and progression free survival (PFS) advantage (90 vs 60 days; HR 0.36; p=0.032) compared to a cohort of patients that had limited exposure to VB-111 (see manuscript by Brenner et al). Radiographic responders to VB-111 exhibited specific imaging characteristics related to its mechanism of action. Survival advantage was also seen in comparison to historic controls, with the percentage of patients living more than one year doubling from 24% to 57%.

The GLOBE Phase 3 study, top-line data from which were announced in 2018, compared upfront concomitant administration of VB-111, without priming, and bevacizumab to bevacizumab monotherapy. In this modified regimen, the treatment did not improve overall survival (OS) and PFS outcomes in rGBM. The new manuscript by Cloughesy et al. attributes the contradictory outcomes between the Phase 2 and Phase 3 trials as being related to the lack of VB-111 monotherapy priming in the GLOBE study, providing clinical, mechanistic and radiographic support for this hypothesis. Notably, GLOBE data show improved outcomes associated with a post VB-111 fever reaction, similar to outcomes from previous VB-111 studies, providing further support that fever is a potential biomarker for better survival with VB-111, secondary to the drug’s immunologic mechanism of action.

"The emerging picture from the Phase 2 and Phase 3 trials points to study regimen as a key factor for ofranergene obadenovec efficacy in rGBM," said Patrick Wen, M.D., Director, Center for Neuro-Oncology at Dana-Farber Cancer Institute, Boston, MA, and a key investigator in both clinical trials. "These results warrant further assessment of ofranergene obadenovec, which we intend to advance in a new randomized, controlled, clinical trial in patients with rGBM undergoing a second surgery."

Details on the new investigator-sponsored Phase 2 trial of VB-111 in rGBM were recently presented at the 2019 Society for Neuro-Oncology Annual Meeting (see link). An investigational new drug application for the new study has already gone into effect with the FDA and study launch is expected in early 2020. VB-111 is also being investigated in a Phase 3 pivotal study in ovarian cancer with interim data expected in the first quarter of 2020.

For a link to the newly published VB-111 papers in Neuro-Oncology refer to: Phase 2 manuscript and Phase 3 manuscript.

On January 8, 2020 Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) reported a publication featured on the cover of Science Translational Medicine describing the potential of a new class of cancer immunotherapy known as "costimulatory bispecific antibodies (Press release, Regeneron, JAN 8, 2020, View Source [SID1234552874])." Regeneron and others have previously shown that CD3 bispecifics can result in meaningful clinical responses in previously untreatable cancer settings. The results published today show that adding a novel class of CD28 costimulatory bispecifics to Regeneron’s CD3 bispecifics can lead to synergistic anti-tumor activity in multiple cell culture and animal model experiments, without inducing systemic cytokine release (cytokine storm).

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"This novel class of CD28 costimulatory bispecifics are key to our strategy of developing a broad oncology portfolio – based on rational combinations to efficiently engage the immune system – to address a broad range of cancers, including those that are not responsive to currently available immunotherapy," said George D. Yancopoulos, M.D., Ph.D., Co-Founder, President and Chief Scientific Officer at Regeneron. "We have dosed prostate cancer patients with our first CD28 costimulatory bispecific, REGN5678, in combination with Libtayo (cemiplimab), and we plan to advance additional CD28 costimulatory bispecifics into the clinic for other cancers this year, including in combinations with CD3 bispecifics."

The rationale for combining CD3 and CD28 bispecific antibodies is based on the fact that T-cells require two signals to fully activate. The first "recognition" signal occurs when the T-cell identifies a foreign or mutated protein (antigen), via its T-cell receptor/CD3 complex. However, the T-cell is only fully activated for cancer cell killing after it receives a second "costimulatory" signal, most powerfully via the CD28 costimulatory receptor. Regeneron’s CD3 and CD28 investigational bispecifics are designed to bridge T-cells to cancer cells and simultaneously provide activation through these two signals. The publication demonstrates that this combination approach can drive markedly enhanced T-cell killing of prostate and ovarian tumors in sophisticated genetically-humanized animal models.

"Cancer researchers have long known that CD28-targeted therapies have the ability to supercharge T-cells against cancer, but little progress was made in harnessing this powerful opportunity given historic safety findings with CD28 superagonists. Our goal was to engage the CD28 pathway in a completely novel and targeted way to avoid the issues with generalized CD28 activation," said Dimitris Skokos, Ph.D., Senior Director, Cancer Immunology Research at Regeneron. "Costimulatory bispecifics offered an innovative solution that allowed us to design antibodies with molecular controls to use CD28 to boost T-cell activation only in the presence of cancer cells and after the ‘recognition’ signal had been received. To see this design work preclinically is gratifying, and we are excited to see if these results will translate in human clinical trials."

CD28 superagonists were investigational CD28-targeted monoclonal antibodies. In a Phase 1 trial conducted in 2006 by another company, a CD28 superagonist overactivated T-cells throughout the bodies of healthy volunteers. This caused life-threatening levels of cytokine release syndrome (known as cytokine storm), leading to multiple organ failure. As a result, clinical research into CD28-based treatments was largely stopped.

This led Regeneron to carefully select CD28 costimulatory bispecific antibody candidates that would only activate T-cells when they were bridged to cancer cells and after having received the first "recognition" signal. Regeneron also tested the safety of its CD28 costimulatory bispecifics in several animal models and showed they did not induce cytokine storm when administered as monotherapy or in combination. These findings support the further investigation of CD28 costimulatory bispecifics in combination with other treatments.

"Checkpoint inhibitors and CAR-T cell therapy have transformed cancer treatment over the past decade, but many patients still don’t respond to these immunotherapies. That’s why it’s exciting to see Regeneron’s CD28 costimulatory bispecifics emerge as promising future off-the-shelf solutions," said Jill O’Donnell-Tormey, Ph.D., Chief Executive Officer and Director of Scientific Affairs at the Cancer Research Institute. "The data published in Science Translational Medicine show that Regeneron is helping to expand the boundaries of what may be possible with immunotherapy."

Among the investigational medicines studied in the paper were two CD28 costimulatory bispecifics (PSMAxCD28 and MUC16xCD28) and two CD3 bispecifics (CD20xCD3 and MUC16xCD3).

About the Regeneron Bispecific Antibody Platform
All of Regeneron’s bispecifics are designed to closely resemble natural human antibodies and bind to two different targets. They are derived from a next-generation version of Regeneron’s proprietary VelocImmune technology and created using the company’s Veloci-Bi platform. These allow for the creation of bispecifics with no linkers or artificial sequences. Additionally, Regeneron bispecifics are manufactured using similar approaches used for human antibody medicines, with similar pharmacokinetics.

There are six Regeneron investigational bispecific antibodies currently in ongoing clinical trials for multiple blood cancers and solid tumors. These bispecifics fall into three categories:

CD3 bispecifics are designed to bridge T-cells and tumor cells. At the tumor site, they activate T-cells via their CD3 receptors and promote T-cell killing of the cancer cells. Investigational candidates include:
CD20xCD3 (REGN1979) for non-Hodgkin B-cell lymphomas;
Two distinct BCMAxCD3s (REGN5458 and REGN5459) for multiple myeloma;
MUC16xCD3 (REGN4018) for ovarian cancer.
CD28 costimulatory bispecifics are also designed to bridge T-cells and tumor cells. At the tumor site, they costimulate T-cells via their CD28 receptors and may synergize with PD-1 inhibitors and/or CD3 bispecifics. Investigational candidates include:
PSMAxCD28 (REGN5678) in combination with Libtayo for prostate cancer.
Tumor-targeted bispecifics are designed to target proteins only on the cancer cell. In this way, they may affect various signaling pathways to hamper the cancer cells’ ability to survive and proliferate. Investigational candidates include:
METxMET (REGN5093) for non-small cell lung cancer that is driven by MET mutations and/or amplifications. REGN5093 targets two different parts of the MET receptor on cancer cells to degrade the receptor and block its ability to trigger cell proliferation.
Regulatory Status of Oncology Programs
The bispecifics mentioned in this release are currently under clinical development, and their safety and efficacy have not been evaluated by any regulatory authority.

Libtayo in combination with REGN5678 is currently under clinical development for prostate cancer, and its safety and efficacy have not been evaluated by any regulatory authority for this use. Libtayo is currently approved in the U.S. for the treatment of patients with metastatic cutaneous squamous cell carcinoma (CSCC) or locally advanced CSCC who are not candidates for curative surgery or curative radiation, and in other countries for similar indications. In the U.S., the generic name for Libtayo is cemiplimab-rwlc, with rwlc as the suffix designated in accordance with Nonproprietary Naming of Biological Products Guidance for Industry issued by the U.S. Food and Drug Administration.

As part of a global collaboration agreement, Regeneron and Sanofi are jointly developing Libtayo, as well as Regeneron’s BCMAxCD3 and MUC16xCD3 bispecific programs.

On January 8, 2020 Molecular Templates, Inc., (Nasdaq: MTEM) a clinical-stage biopharmaceutical company focused on the discovery and development of the Company’s proprietary targeted biologic therapeutics, engineered toxin bodies (ETBs), reported that provided a corporate update and outlined expected 2020 milestones (Press release, Molecular Templates, JAN 8, 2020, View Source [SID1234552841]).

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"2019 was a year of growth for MTEM as we advanced our pipeline programs, established a new collaboration outside of oncology with a premier partner, and strengthened our balance sheet with a successful equity financing," said Eric Poma, Ph.D., Chief Executive and Chief Scientific Officer of Molecular Templates. "As we start 2020, we look forward to generating clinical data from three ongoing Phase 2 studies with MT-3724, an ongoing Phase 1 study for MT-5111, and a Phase 1 study with TAK-169. We expect to file an IND in 2H20 for MT-6402, our PD-L1-targeted ETB with antigen seeding capabilities, and we will continue to advance our earlier stage pipeline while making progress with our existing collaborations."

2019 Accomplishments, Status Updates, and Expected 2020 Milestones

MT-3724 (CD20 ETB)

Candidate description
MT-3724 is a 1st generation ETB that utilizes wild-type Shiga-like toxin A (SLTA) genetically fused to an scFv to CD20 to bind, induce internalization, and destroy CD20-expressing tumor cells through ribosomal inactivation.
2019 accomplishments
In 2019, MTEM presented final results of the Phase 1/1b monotherapy study in lymphoma patients and initiated three Phase 2 studies in diffuse large B-cell lymphoma (DLBCL); a monotherapy study that has the potential to be pivotal and two combination studies, one with lenalidomide and the other with gemcitabine/oxaliplatin (GemOx).
The final Phase 1/1b results presented at the American Society of Hematology (ASH) (Free ASH Whitepaper) annual meeting included safety data on doses from 5-100 μg/kg, and efficacy data on 13 serum rituximab negative (RTX-neg) DLBCL or mixed DLBCL/FL subjects of whom 5 responded (38% objective response rate) across the range of 5 to 50 μg/kg doses. Of the 5 responses, 2 were complete responses (CRs) and 3 were partial responses (PRs). Three patients had stable disease (including 2 patients with 49% and 47% tumor reductions) and 5 patients had progressive disease. Of the 5 serum RTX-neg subjects with DLBCL who received MT-3724 at 50 μg/kg, the maximum tolerated dose (MTD), 3 responded (2 CRs, 1 PR).
The combination study with lenalidomide has demonstrated preliminary evidence of tolerability and efficacy with lenalidomide at standard doses and MT-3724 at 10 μg/kg. MT-3724 dosing at 25 μg/kg with lenalidomide is ongoing.
The combination study with GemOx has demonstrated preliminary evidence of efficacy but grade 2 innate immune adverse effects were seen with standard doses of gemcitabine and oxaliplatin and 10 μg/kg doses of MT-3724. The study protocol has been amended to include a revised schedule where MT-3724 dosing is initially sequenced with GemOx dosing.
Status updates and expected 2020 milestones
The potentially pivotal Phase 2 monotherapy DLBCL study is ongoing and is planned to enroll up to 100 patients. MTEM expects to announce updates on interim clinical results from this study and the ongoing lenalidomide and GemOx combination studies throughout 2020.
MT-5111 (HER2 ETB)

Candidate description
MT-5111 is a 2nd generation ETB technology that utilizes a genetically engineered de-immunized Shiga-like toxin A-subunit (SLTA) to reduce the potential for innate and adaptive immunogenicity. MT-5111 directly kills HER2-positive cells via ribosomal inactivation, a mechanism wholly distinct from approved HER2 targeted agents.
MT-5111 binds HER2 in the presence of trastuzumab and pertuzumab, creating the possibility of combining MT-5111 with other HER2 antibody-based agents.
MT-5111 is 55 kDa, almost a third smaller than traditional antibody and antibody drug conjugate (ADC) therapies, and, because of its smaller size, may have superior tumor penetration.
2019 accomplishments
In 2019, the IND for MT-5111 was accepted by the FDA and MTEM initiated a Phase 1 study, for which dosing began in 4Q19. MTEM also presented preclinical data on MT-5111 at the San Antonio Breast Cancer Symposium (SABCS).
Status update and expected 2020 milestones
The Phase 1 study is ongoing with multiple sites open for enrollment. MTEM expects to announce interim clinical results from this study in 2Q20 and additional data from the dose escalation portion of the study in 4Q20.
TAK-169 (CD38 ETB)

Candidate description
TAK-169 is a 2nd generation ETB that utilizes a genetically engineered de-immunized Shiga-like toxin A-subunit (SLTA) to reduce the potential for innate and adaptive immunogenicity. TAK-169 targets CD38, a poorly internalizing receptor expressed on myeloma cells, and directly kills CD38-expressing tumor cells via ribosomal inactivation.
Data in non-human primates suggest that TAK-169 can be dosed at higher doses than MT-3724 with a markedly reduced propensity of innate immune response compared with MT-3724.
Preclinical data suggest that TAK-169 retains activity in the presence of daratumumab, an approved CD38 antibody.
2019 accomplishments
In 2019, MTEM and partner Takeda presented preclinical data on TAK-169 at the American Association of Cancer Research (AACR) (Free AACR Whitepaper) annual meeting, the IND for TAK-169 was accepted by the FDA, and Takeda initiated a Phase 1 study in relapsed/refractory multiple myeloma in 4Q19. In December 2019, TAK-169 received Orphan Drug Designation from the FDA.
Status update
Multiple sites are open for enrollment.
MT-6402 (PD-L1 ETB)

Candidate description
MT-6402 is a 3rd generation ETB that targets PD-L1, a poorly internalizing receptor expressed on various solid tumors. MT-6402 shares the de-immunized scaffold used with 2nd-generation ETBs and is further engineered to deliver a viral foreign class I peptide (antigen seeding) to alter the tumor immunophenotype.
MT-6402 utilizes Antigen Seeding Technology to deliver a foreign class I antigen derived from cytomegalovirus (CMV) inside the tumor for presentation on the tumor cell surface in complex with MHC class I molecules. MTEM has shown that antigen seeding allows CMV-reactive T-cells to recognize and destroy tumor cells. This T-cell response provides a mechanism of cell kill that is complementary to the ribosomal inactivation caused by the SLTA.
2019 accomplishments
In 2019, MTEM presented preclinical data on its PD-L1 targeted ETBs at the AACR (Free AACR Whitepaper) and Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) annual meetings demonstrating potent anti-tumor effects on PD-L1+ tumor cells, good safety and pronounced pharmacodynamic effects in non-human primates, and a unique ability to alter the immunophenotype of tumors cells through antigen seeding.
Status update and expected 2020 milestones
An IND is expected to be filed and the Phase 1 study for MT-6402 is expected to be initiated in 2H20.
Earlier stage pipeline

Status update and expected 2020 milestones
MTEM continues to work on discovery of new ETBs against targets including CTLA-4, SLAMF-7, and CD45.
In 2020, MTEM expects to present preclinical data on new targets and new ETBs at conferences.
Corporate and Business Development

2019 accomplishments
On November 18, 2019, MTEM and Vertex Pharmaceuticals announced a strategic research collaboration to discover and develop novel targeted conditioning regimens that may enhance the hematopoietic stem cell transplant process, including transplants conducted as part of treatment with ex vivo CRISPR/Cas9 gene editing therapies such as CTX001. Under the collaboration, MTEM will conduct research activities for the use of ETBs for up to two targets selected by Vertex. The initial research will be focused on discovering a novel conditioning regimen using MTEM’s ETB technology platform. In addition, Vertex has an option to select a second target as part of the collaboration. Vertex made an up-front payment of $38 million to MTEM, including an equity investment. MTEM is also eligible to receive future development, regulatory and sales milestones and option payments of up to $522 million (across two targets) and tiered royalty payments on future sales.
On November 21, 2019, MTEM announced the pricing of an underwritten equity offering, the net proceeds of which were approximately $53.3 million, after deducting underwriting discounts and commissions and other estimated offering expenses payable by MTEM.
Status update and expected 2020 milestones
MTEM has three ongoing collaborations: the co-development collaboration with Takeda for TAK-169, the multi-target collaboration with Takeda for the discovery and development of new ETBs against two undisclosed oncology targets, and the multi-target collaboration with Vertex for the discovery and development of new conditioning regimens. All three of these collaborations are expected to advance in 2020.

On January 8, 2020 Verastem, Inc. (Nasdaq:VSTM) (Verastem Oncology or the Company), a biopharmaceutical company focused on developing and commercializing medicines seeking to improve the survival and quality of life of cancer patients, reported a global licensing agreement with Chugai Pharmaceutical Co., Ltd., (Chugai) whereby Verastem Oncology is obtaining worldwide development and commercialization rights to the RAF/MEK inhibitor CH5126766 (CKI27) from Chugai currently under development for the treatment of KRAS mutant solid tumors (Press release, Verastem, JAN 8, 2020, View Source [SID1234552858]). The Company will host an investor call to discuss the opportunity and a development update today (details below).

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CH5126766 in combination with Verastem Oncology’s focal adhesion kinase (FAK) inhibitor, defactinib, is currently the subject of a clinical study (Phase I followed by expansion cohorts) with the expansion cohorts now ongoing in patients with KRAS mutant advanced solid tumors, including low grade serous ovarian cancer (LGSOC), non-small cell lung cancer (NSCLC) and colorectal cancer (CRC).1 This clinical study of the defactinib/CH5126766 combination is supported by the single-agent Phase 2 studies of defactinib in KRAS mutant NSCLC2 and CH5126766 in KRAS mutant NSCLC and LGSOC.3

"Based on the single-agent defactinib results in KRAS mutant NSCLC, we conducted an internal pre-clinical effort to identify drug classes that were synergistic with defactinib and saw the highest level of synergy in combination with MEK inhibitors and, specifically, with CH5126766," said Dan Paterson, President and Chief Operating Officer of Verastem Oncology. "The exciting early clinical results led to our decision to enter into a partnership with Chugai for CH5126766 and accelerate the combination development program for patients with KRAS mutant cancers, which are highly aggressive and recurrent. We plan to initiate discussions with regulatory authorities about our development plans and to define the registration path early this year."

"We found that MEK blockade activates FAK signaling as a potential escape mechanism," stated Professor Udai Banerji, Professor of Molecular Cancer Pharmacology at The Institute of Cancer Research and Honorary Consultant in Medical Oncology, MBBS, MD, DNB, PhD, FRCP at The Royal Marsden NHS Foundation Trust, London, England, and lead investigator of the clinical study. "Based on the synergy between FAK and MEK inhibitors observed in preclinical KRAS mutant models, we have been assessing the combination of defactinib and CH5126766 for treatment of patients with KRAS mutant cancers. The results to date have been encouraging and we look forward to sharing our clinical findings, including the response rate in an upcoming scientific presentation."

"CH5126766 is a unique and particularly promising inhibitor of the RAS/RAF/MEK signaling pathway," noted Neal Rosen, MD, PhD, Memorial Sloan Kettering Cancer Center, NY, NY. "In contrast to other MEK inhibitors in development, CH5126766 blocks both MEK kinase activity and the ability of RAF to phosphorylate MEK. This unique mechanism allows CH5126766 to block MEK signaling without the compensatory activation of MEK that appears to limit the efficacy of other inhibitors. The clinical data with the combination of defactinib and CH5126766 are striking and suggest promise for patients with KRAS mutant solid tumors."

Under the terms of the agreement, Verastem Oncology is responsible for the development and worldwide commercialization of CH5126766. The Company will make an upfront payment of $3M and pay royalties to Chugai. Given the potential of the opportunity, the Company will be evaluating various partnering strategies.

Conference Call and Webcast Information

The Verastem Oncology management team will host a conference call and webcast on Wednesday, January 8, 2020, at 4:00 PM (ET). The call can be accessed by dialing (877) 341-5660 (U.S. and Canada) or (315) 625-3226 (international), five minutes prior to the start of the call and providing the passcode 3756707 and web PIN 1655.

The live, listen-only webcast of the conference call can be accessed by visiting the investors section of the Company’s website at View Source A replay of the webcast will be archived on the Company’s website for 90 days following the call.

About Defactinib

Defactinib is an oral small molecule inhibitor of FAK and PYK2 that is currently being evaluated as a potential combination therapy for various solid tumors. The Company has received orphan drug designation for defactinib in ovarian cancer and mesothelioma in the US, EU and Australia. Preclinical research by Verastem Oncology scientists and collaborators at world-renowned research institutions has described the effect of FAK inhibition to enhance immune response by decreasing immuno-suppressive cells, increasing cytotoxic T cells, and reducing stromal density, which allows tumor-killing immune cells to enter the tumor.4,5 A Phase 1/2 clinical trial of defactinib in combination with CH5126766 in patients with KRAS mutant advanced solid tumors, including low grade serous ovarian cancer (LGSOC), non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) is underway.1 The defactinib/CH5126766 combination is supported by the single-agent Phase 2 studies of defactinib in KRAS mutant NSCLC2 and CH5126766 in KRAS mutant NSCLC and LGSOC.3 Defactinib is also in clinical testing in combination with pembrolizumab for treatment of patients with pancreatic cancer, NSCLC and mesothelioma.6

On January 8, 2020 Medicenna Therapeutics Corp. ("Medicenna" or the "Company") (TSX: MDNA;OTCQB: MDNAF), a clinical stage immuno-oncology company, reported that it has received $1,345,871 from the early exercise of previously issued warrants (Press release, Medicenna Therapeutics, JAN 8, 2020, View Source [SID1234552875]). A total of 855,621 warrants were exercised, with exercise prices ranging from $1.20-$2.00. The proceeds of the warrant exercises will be used towards the development of Medicenna’s long-acting IL-2 superkine (MDNA19) and for general and working capital purposes.

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"This early exercise of warrants is a clear indicator of the confidence that investors have in Medicenna and our short and long-term opportunities," says Fahar Merchant, President and Chief Executive Officer of Medicenna. "Combined with our recent oversubscribed financing, these funds provide us with a robust balance sheet that will see us through important upcoming milestones, including the completion of a full MDNA55 data set and subsequent meeting with the FDA, the ongoing advancement of our best-in-class IL-2 asset MDNA19 and our ongoing operations into 2021."

The exercises consist of 274,000 warrants priced at $1.20 and expiring December 21, 2023, 526,621 warrants priced at $1.75 and expiring October 17, 2022, 5,000 warrants priced at $1.20 and expiring December 21, 2020, 15,000 warrants priced at $1.30 and expiring October 17, 2021 and 35,000 warrants priced at $2.00 and expiring April 5, 2021. The number of issued and outstanding common shares following the exercises is 34,991,097.