On December 13, 2021 CTI BioPharma Corp. (Nasdaq: CTIC) reported that five scientific poster presentations on the pacritinib clinical program at the 63rd American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting & Exposition, being held as a hybrid (virtual and live) meeting in Atlanta, Georgia, December 11-14, 2021 (Press release, CTI BioPharma, DEC 13, 2021, View Source [SID1234596916]).

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"We are pleased with the growing body of clinical evidence supporting the potential of pacritinib’s unique place in treating cytopenic myelofibrosis, specifically in patients with moderate or severe thrombocytopenia, a notable challenge in light of the significant limitations of approved therapies," said Adam R. Craig, M.D., Ph.D., President and Chief Executive Officer of CTI BioPharma. "Importantly, today we presented data demonstrating that in patients with cytopenic myelofibrosis, full-dose pacritinib yielded higher response rates and a similar safety profile to lower doses of ruxolitinib. Prolonged administration of pacritinib is possible with favorable tolerability in the compassionate use setting, and the use of pacritinib can lead to significant overall and individual symptom relief in patients with both moderate and severe thrombocytopenia."

"As we approach our PDUFA action date of February 28, 2021, we remain focused on bringing forward a new therapeutic option for patients with cytopenic myelofibrosis through our committed collaboration with the FDA."

All presentation materials will be available at ctibiopharma.com.

A Retrospective Head-to-Head Comparison between Pacritinib and Ruxolitinib in Patients with Myelofibrosis and Moderate to Severe Thrombocytopenia (ASH Poster #3639)

Pacritinib, a JAK 2/interleukin-1 receptor–associated kinase 1 (IRAK1) inhibitor that does not inhibit JAK1, is in development for use in patients with myelofibrosis who have thrombocytopenia. Pacritinib was studied in thrombocytopenic patients (platelet count ≤100 x 109/L) in the randomized phase 3 PERSIST-2 trial, which showed pacritinib was superior to best available therapy (BAT), including ruxolitinib, based on spleen volume reduction (SVR) and modified total symptom score (mTSS) response. While many patients in the BAT arm (45%) received ruxolitinib, an analysis of the comparison between pacritinib and ruxolitinib has not been previously performed.

This retrospective head-to-head analysis of pacritinib versus ruxolitinib in "first-line" (ruxolitinib-naïve) patients treated in PERSIST-2 showed that patients with moderate or severe thrombocytopenia were able to maintain full dose intensity with pacritinib. Pacritinib fully dosed at 400 mg/day resulted in numerically higher rates of SVR (28% vs 11%) and mTSS response (37% vs 11%), and a similar safety profile compared with lower doses of ruxolitinib in "first-line" patients with cytopenic myelofibrosis, suggesting that pacritinib may address the unmet medical need of patients with cytopenic myelofibrosis who cannot tolerate full doses of JAK1/2 inhibitors, such as ruxolitinib.

Safety Analysis of Pacritinib in Patients with Myelofibrosis and Severe Thrombocytopenia (ASH Poster #3640)

Pacritinib, a novel JAK2/IRAK1 inhibitor, demonstrated clinically significant activity in spleen volume and symptom reduction in patients with advanced cytopenic myelofibrosis, including those with severe thrombocytopenia (platelet count <50 x 109/L), in phase 2 and 3 clinical trials. Pacritinib, unlike JAK1/2 inhibitors, has demonstrated clinical benefit at the recommended full dose of 200 mg twice daily (BID) in patients with cytopenias in the phase 2 dose–finding PAC203 and phase 3 PERSIST-2 trials.

In this retrospective safety analysis of patients with cytopenic myelofibrosis, including those who had severe thrombocytopenia, the safety profile of pacritinib 200 mg BID was comparable to best available therapy (BAT), which included non-therapeutic options (i.e. supportive care and watch and wait). This analysis suggests that pacritinib 200 mg BID may represent the first fully dosed therapeutic option for patients with cytopenic myelofibrosis, including severe thrombocytopenia.

Long-Term Treatment with Pacritinib on a Compassionate Use Basis in Patients with Advanced Myelofibrosis (ASH Poster #3640)

The efficacy and safety of pacritinib has been evaluated in multiple clinical trials, including two randomized, controlled phase 3 trials (PERSIST-1 and PERSIST-2) and a phase 2 dose-finding trial (PAC203). These trials are unique in the myelofibrosis landscape because they enrolled patients with advanced disease and severe cytopenias. When these trials closed, patients who received pacritinib could apply to continue treatment on a compassionate use basis. This analysis describes pacritinib treatment in this program.

Patients who were treated with pacritinib on PERSIST-1, PERSIST-2, or PAC203 were provided the option to continue receiving pacritinib if they were eligible for the compassionate use program. After receiving pacritinib on an original clinical trial, 75 patients continued to receive pacritinib on a compassionate use basis. Twenty patients were still on pacritinib as of the data cutoff date. Most patients had advanced disease, characterized by cytopenias and circulating blasts.

Median total combined treatment duration (original trial and compassionate use) was 21.1 months (range 0.8 to 80.9 months). Among patients with prior JAK inhibitor exposure, median time from discontinuation from a JAK inhibitor to the last day of known treatment with compassionate use pacritinib was 27.2 months. This duration compares favorably to median survival reported in patients discontinuing ruxolitinib: 14 months overall and about 8 months if the platelet count is <100×109/L.. Prolonged treatment with pacritinib is well-tolerated in patients with advanced myelofibrosis, including those with cytopenias, and reported serious adverse events were consistent with those expected in advanced myelofibrosis patient population and with treatment in a compassionate use setting.

The Impact of Pacritinib on Myelofibrosis Symptoms in Patients with Moderate and Severe Thrombocytopenia: A Retrospective Analysis of Patients in the Persist-2 Trial (ASH Poster #3628)

Pacritinib demonstrated superior spleen volume response versus BAT in patients with myelofibrosis who have moderate or severe thrombocytopenia (platelet count ≤100 x 109/L) in the phase 3 PERSIST-2 trial. Unlike the trials in which JAK1/2 inhibitors were approved, which relied on a modified TSS (mTSS) score that excluded "tiredness," PERSIST-2 included tiredness as part of the TSS.

This retrospective analysis showed that significantly more patients achieved a mTSS response with pooled pacritinib versus BAT (31% vs 14%; P=0.008). More patients achieved a mTSS response with pacritinib 200 mg BID versus BAT (35% vs 14%; P=0.004) and BAT=RUX (35% vs 19%; P=0.110). Patients in the pacritinib 200 mg BID arm experienced greater percent reductions in individual myelofibrosis symptoms between baseline and week 24 compared with BAT, and the severity of physical function symptoms were reduced more with pacritinib 200 mg BID compared with BAT by week 24.

Evidence of NF-ΚB Pathway Activation in Patients with Advanced, High Molecular Risk Myelofibrosis (ASH Poster #3584)

Patients with myelofibrosis who discontinue treatment with ruxolitinib have a poor prognosis that is often associated with advanced phases of disease and severe cytopenias. While these patients are more likely to have high molecular risk (HMR) genomic markers, biological drivers of disease in this advanced population are not well characterized. The interaction between high-risk mutations and cytokine profiles of patients treated in PAC203 were retrospectively analyzed.

In this HMR+ and RAS mutant-enriched cohort of myelofibrosis patients who were intolerant of or resistant to ruxolitinib, a relationship between HMR mutations and an NF-kB directed pro-inflammatory cytokine signature was identified. These results implicate the activation of a distinct biological signaling pathway operative in this molecularly-defined cohort.

About Myelofibrosis and Cytopenias
Myelofibrosis is a bone marrow cancer that results in the formation of fibrous scar tissue and can lead to thrombocytopenia and anemia, weakness, fatigue and an enlarged spleen and liver. Within the U.S. there are approximately 21,000 patients with myelofibrosis, 7,000 of which have severe thrombocytopenia (defined as blood platelet counts of less than 50 x109/L). Severe thrombocytopenia is associated with poor survival and high symptom burden and can occur as a result of disease progression or from drug toxicity with other JAK2 inhibitors such as JAKAFI and INREBIC.

About Pacritinib
Pacritinib is an investigational oral kinase inhibitor with specificity for JAK2, IRAK1 and CSF1R, but not JAK1. The JAK family of enzymes is a central component in signal transduction pathways, which are critical to normal blood cell growth and development, as well as inflammatory cytokine expression and immune responses. Mutations in these kinases have been shown to be directly related to the development of a variety of blood-related cancers, including myeloproliferative neoplasms, leukemia and lymphoma. In addition to myelofibrosis, the kinase profile of pacritinib suggests its potential therapeutic utility in conditions such as acute myeloid leukemia (AML), myelodysplastic syndrome (MDS), chronic myelomonocytic leukemia (CMML) and chronic lymphocytic leukemia (CLL), due to its inhibition of c-fms, IRAK1, JAK2 and FLT.

On December 13, 2021 NexImmune, Inc. (Nasdaq: NEXI), a clinical-stage biotechnology company developing a novel approach to immunotherapy designed to orchestrate a targeted immune response by directing the function of antigen-specific T cells, reported preliminary Phase 1/2 results from an ongoing study of NEXI-002, a patient-derived multi-antigen-specific CD8+ T cell treatment for patients with relapsed/refractory multiple myeloma who have failed ³3 prior lines of therapy (Press release, NexImmune, DEC 13, 2021, View Source [SID1234596933]). The data on low doses of NEXI-002, presented at the 63rd American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition, showed a promising safety and tolerability profile and evidence of immunologic and clinical activity.

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Poster Presentation:

Title: Preliminary Analysis of a Phase 1/2 Study of NEXI-002 Autologous Multi-Antigen-Specific CD8+ T cells for the Treatment of Relapsed or Refractory Multiple Myeloma (RRMM)

Abstract Number: 2824

Category: Poster Presentation

Authors: Maung Myo Htut, MD, Juan C. Varela, MD, PhD, Vineetha Edavana, PhD, Emily Lu, PhD, Sojung Kim, PhD, Lauren Suarez, PhD, Mathias Oelke, PhD, Daniel Bednarik, PhD, Robert D. Knight, MD, and, Andrew Kin, MD

Date & Time: Sunday, December 12, 2021; Poster Hall Hours 6-8 pm EDT

In this heavily pre-treated patient group (n=6 with an average of 7.6 lines of prior therapy), the clinical data suggests that NEXI-002 is well-tolerated without dose-limiting toxicities (no grade ³3 CRS or any grade of ICANS). Biomarker data show that the NEXI-002 product candidate contains CD8+ antigen-specific T cells with key memory phenotypes which, after administration, are detected in peripheral blood and bone marrow of treated individuals and proliferate and persist over time. Furthermore, TCR sequencing shows that the NEXI-002 product candidate contains CD8+ T cell clones that were undetectable in the peripheral blood of the patients at baseline and which expand in both blood and bone marrow over time. After receiving lymphodepleting therapy followed by NEXI-002 infusion, patients

experienced rapid lymphocyte recovery with reconstitution of both CD4+ and CD8+ T cell subtypes. Despite the infusion of very low numbers of NEXI-002 T cells (4-10x10e6 total T cells), these heavily pre-treated patients achieved stable disease for 2 to 3.5 months of duration. Importantly, despite receiving an average of 7.6 previous lines of therapy, the quality, functionality and in vivo persistence of all patient-derived NEXI-002 T cell products were comparable to those expanded from healthy donors. Strategies to yield higher product doses are underway, including evaluating patients with lower disease burden plasma cell dyscrasias.

"We are very encouraged by the initial Phase 1/2 results observed to-date with NEXI-002," said Scott Carmer, CEO of NexImmune. "We have now shown, in two separate clinical trials using apheresis material from either healthy donors or heavily pre-treated patients, that we can manufacture CD8+ T cell products with high target antigen specificity and with T cell phenotypes that promote in vivo proliferation, persistence and anti-tumor activity. Even at the very low doses of NEXI-002 administered in this ongoing trial, we’ve seen robust biomarker and immunological responses with evidence of clinical activity. These preliminary data provide further evidence of the NEXI-002 mechanism of action, and we are eager to continue assessing NEXI-002’s potential in this patient population and in additional patients with lower-disease-burden plasma cell dyscrasias."

On December 13, 2021 Affimed N.V. (Nasdaq: AFMD), a clinical-stage immuno-oncology company committed to giving patients back their innate ability to fight cancer, reported that preclinical data from two of their Innate Cell Engager (ICE) programs at the 63rd American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting (ASH) (Free ASH Whitepaper) (Press release, Affimed, DEC 13, 2021, View Source [SID1234596964]). The poster presentations included preclinical proof-of-concept data on AFM28, for which Affimed recently revealed the target and indication. The program is in development for the treatment of Acute Myeloid Leukemia and other CD123+ hematologic malignancies. The second poster presentation provided data on the activity of AFM13 pre-complexed to NK cells after cryopreservation, demonstrating the potential to develop AFM13 as an off-the-shelf chimeric antigen receptor (CAR)-like NK cell product.

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Preclinical characterization of the ICE AFM28

The novel ICE AFM28 is designed to target CD16A on innate immune cells and CD123 on tumor cells in relapsed or refractory acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). CD123 is almost universally expressed on leukemic blasts and leukemic stem cells (LSCs) and thereby represents a promising target in both indications.

The results revealed that target cell lysis via NK cell-mediated antibody-dependent cell-mediated cytotoxicity (ADCC), even at low CD123 expression, was more pronounced compared to conventional anti-CD123 antibodies. In addition, AFM28 showed a 100-fold more potent NK cell activation in an ex vivo analysis, compared to Fc-enhanced IgG1 antibodies. When compared with a CD123-targeting T cell-engaging bispecific antibody, AFM28 activity was associated with substantially lower levels of inflammatory cytokine release suggesting low risk of cytokine release syndrome. In support of these findings, administration of AFM28 to cynomolgus monkeys induced the effective depletion of CD123+ target cells and was well tolerated.

AFM28 is currently being prepared for clinical evaluation. The properties of the preclinical characterization make it an interesting candidate for combination approaches with allogeneic NK cell products.

"There is an urgent need for relapsed or refractory AML and MDS patients and targeting the innate immune system – either alone or in combination with adoptive NK cells – holds promise for these patients," said Dr. Arndt Schottelius, CSO of Affimed. "Our data suggests that AFM28 engages NK cells to lyse CD123-positive leukemic blasts and leukemic stem cells. This is a critical step in achieving long-lasting remissions."

Cryopreservation of NK cells pre-complexed with innate cell engagers (CAR-like NK cells)

Pre-complexing NK cells with the ICE AFM13 generates chimeric antigen receptor (CAR)-like NK cells. Our preclinical assays demonstrate that anti-tumor efficacy of AFM13 pre-complexed NK cells was comparable to NK cells that were combined, though not pre-complexed with AFM13. Furthermore, the data showed that tumor cell lysis was enhanced compared to a Fc-enhanced antibody approach.

Retaining biological activity and specificity after cryopreservation is a prerequisite to enable the development of pre-complexed off-the-shelf CAR-like NK cell products. Our results confirmed that the efficacy of tumor cell lysis by AFM13-pre-complexed NK cells, was virtually unaffected after one cycle of cryopreservation at -80°C.

"The data are the basis to develop an off-the-shelf precomplexed NK cell product of our ICE molecules and mark an important milestone," said Dr. Arndt Schottelius, CSO of Affimed. "This is especially encouraging as we recently announced very promising data of the Phase 1-2 study at The University of Texas MD Anderson Cancer Center that evaluates AFM13 pre-complexed with NK cells in patients with CD30-positive lymphomas revealing a 100% objective response rate in 13 patients who received the recommended phase 2 dose."

The poster will additionally be featured on December 15 at 5:00 pm ET in the virtual poster walk on Natural Killer Cell-Based Immunotherapy which can be accessed via the following link: View Source

The full posters are available on Affimed’s website under "Publications & Posters". For more details about the ASH (Free ASH Whitepaper) Virtual Annual Meeting please visit: View Source

About AFM28

AFM28, a tetravalent, bispecific CD123- and CD16A-binding ICE developed on Affimed’s ROCK platform, is designed to bring a new immunotherapeutic approach to patients with CD123+ myeloid malignancies, including acute myeloid leukemia and myelodysplastic syndrome (MDS). It engages NK cells to initiate tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC), even at low CD123 expression levels. Clinical development is planned as both monotherapy and in combination with allogeneic NK cells in patients with relapsed/refractory CD123+ leukemias.

About AFM13

AFM13 is a first-in-class ICE that uniquely activates the innate immune system to destroy CD30-positive hematologic tumors. AFM13 induces specific and selective killing of CD30-positive tumor cells, leveraging the power of the innate immune system by engaging and activating NK cells and macrophages. AFM13 is Affimed’s most advanced ICE clinical program and is currently being evaluated as a monotherapy in a registration-directed trial in patients with relapsed/refractory peripheral T-cell lymphoma or transformed mycosis fungoides (REDIRECT). The study is actively recruiting, and additional details can be found at www.clinicaltrials.gov (NCT04101331).

In addition, The University of Texas MD Anderson Cancer Center is studying AFM13 in an investigator-sponsored phase 1 trial in combination with cord blood-derived allogeneic NK cells in patients with relapsed/refractory CD30-positive lymphomas (NCT04074746).

On December 13, 2021 IceCure Medical Ltd. (NASDAQ: ICCM) (TASE: ICCM) (the "Company" or "IceCure"), developer of minimally-invasive cryoablation technology, the ProSense System, that destroys tumors by freezing as an alternative to surgical tumor removal, reported the closing of its underwritten public offering of 3,892,152 shares of the Company’s ordinary shares, inclusive of 578,325 shares offered pursuant to the underwriters’ over-allotment option, at a price to the public of $3.45 per share, before underwriting discounts and commissions, and to certain investors in lieu of ordinary shares, pre-funded warrants to purchase up to an aggregate of 1,034,000 ordinary shares at a price to the public of $3.449 per pre-funded warrant, which represents the per share public offering price for the Ordinary Shares less the $0.001 per share exercise price for each such pre-funded warrant (Press release, IceCure Medical, DEC 13, 2021, View Source [SID1234596986]). The gross proceeds of the offering to the Company were approximately $17 million, before deducting underwriting discounts, commissions, and other offering expenses.

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A.G.P./Alliance Global Partners acted as sole book-running manager for the offering. Brookline Capital Markets, a division of Arcadia Securities, LLC, acted as a co-manager for the offering.

The Company intends to use the net proceeds from the offering for new product development, business development, working capital and general corporate purposes.

The offering was made by means of a prospectus. A copy of the final prospectus related to the offering may be obtained from A.G.P./Alliance Global Partners, 590 Madison Avenue, 28th Floor, New York, NY 10022, or by telephone at (212) 624-2060, or by email at [email protected] or by visiting EDGAR on the SEC’s website at www.sec.gov.

A registration statement relating to these securities was filed with the Securities and Exchange Commission and declared effective on December 8, 2021. This press release shall not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction.

On December 13, 2021 ORIC Pharmaceuticals, Inc. (Nasdaq: ORIC), a clinical stage oncology company focused on developing treatments that address mechanisms of therapeutic resistance reported that preclinical data with ORIC’s small molecule inhibitor of CD73 in multiple myeloma at the American Society of Hematology (ASH) (Free ASH Whitepaper), in collaboration with Dr. Kenneth Anderson’s research laboratory at Dana-Farber Cancer Institute (Press release, ORIC Pharmaceuticals, DEC 13, 2021, View Source [SID1234597018]). The abstract and presentation are available for online viewing via the ASH (Free ASH Whitepaper) Annual Meeting website.

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"ORIC-533 has a differentiated profile, demonstrating stronger potency in a high AMP environment compared to benchmark CD73 inhibitors and adenosine receptor antagonists in preclinical studies," said Lori Friedman, chief scientific officer. "Based on a strong mechanistic rationale and compelling single agent activity in patient-derived autologous ex vivo assays, we are excited to pursue clinical development in multiple myeloma."

Multiple myeloma patient samples have demonstrated that the tumor environment is adenosine rich, and studies have shown that high CD73 and adenosine levels are associated with poor prognosis and therapeutic resistance.

The ASH (Free ASH Whitepaper) presentation focused on the role of adenosine signaling in immunosuppression in patients with relapsed or refractory multiple myeloma and the ability of ORIC’s small molecule inhibitor of CD73 to restore antitumor immune activity.

Key highlights from a series of experiments utilizing bone marrow aspirates from patients with multiple myeloma include:

CD73 inhibition addressed adenosine mediated immunosuppression, which stimulated T-cell proliferation, T-cell activation, and activation of plasmacytoid dendritic cells in ex vivo assays derived from patients with multiple myeloma.
ORIC’s small molecule inhibitor of CD73 overcame immunosuppression and triggered significant lysis and cell death of multiple myeloma cells by autologous T-cells from the bone marrow microenvironment.
ORIC’s CD73 inhibitor demonstrated single agent activity, comparing favorably to standard of care therapies, in bone marrow-derived mononuclear cell assays from relapsed or refractory myeloma patients.
The company plans to pursue a single agent clinical development plan for ORIC-533 in multiple myeloma and initiate a Phase 1 trial in the fourth quarter of 2021.

Additional Pipeline Updates:

ORIC-114 EGFR/HER2 Inhibitor

ORIC-114 is a brain penetrant, orally bioavailable, irreversible inhibitor designed to selectively target EGFR and HER2 with high potency against exon 20 insertion mutations. The company recently disclosed that ORIC-114 induced tumor regressions in a subcutaneous HER2 positive breast cancer xenograft model. In a new study, ORIC-114 demonstrated significant tumor growth inhibition in an intracranial HER2 positive breast cancer model, with superior antitumor activity versus tucatinib. The CTA has been filed in South Korea, and initiation of a Phase 1 trial is expected in early 2022.

ORIC-944 PRC2 Inhibitor

ORIC-944 is a potent and selective allosteric inhibitor of polycomb repressive complex 2 (PRC2) that targets its regulatory embryonic ectoderm development (EED) subunit and has demonstrated single agent efficacy in multiple enzalutamide-resistant prostate cancer models in preclinical studies. The IND was cleared by the FDA in December, and initiation of a Phase 1 trial is expected in early 2022.

Webcast and Conference Call Details

ORIC will host a conference call and webcast, today at 5:30 p.m. ET. To participate in the conference call, please dial (833) 651-0991 (domestic) or (918) 922-6080 (international) and refer to conference ID 7989199. A live webcast and audio archive of the conference call will be available through the investor section of the company’s website at www.oricpharma.com. The webcast will be available for replay for 90 days following the presentation.

About ORIC-533

ORIC-533 is a highly potent, orally bioavailable small molecule inhibitor of CD73, a key node in the adenosine pathway believed to play a central role in resistance to chemotherapy and immunotherapy-based treatment regimens. ORIC-533 has demonstrated greater potency in preclinical studies compared to an antibody approach, as well as other small molecule inhibitors of CD73 and adenosine receptor antagonists. Preclinical data demonstrated that ORIC-533 binds CD73 with high affinity and effectively blocks adenosine-driven immunosuppression in a high AMP environment, reflective of AMP levels observed in tumors. In preclinical studies, nanomolar concentrations of ORIC-533 efficiently rescued cytotoxic T-cell function in the presence of high AMP concentrations, as well as in ex vivo bone marrow aspirates from relapsed or refractory multiple myeloma patients.