On November 9, 2018 Celldex Therapeutics, Inc. (NASDAQ:CLDX) reported interim data Phase 1 dose-escalation study of CDX-1140, a fully human agonist anti-CD40 antibody (Press release, Celldex Therapeutics, NOV 9, 2018, View Source [SID1234531094]). CD40, expressed on dendritic cells and other antigen presenting cells, has long been an important target for immunotherapy, as it plays a critical role in the activation of innate and adaptive immune responses. The data were presented in a poster session at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) 33rd Annual Meeting.

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"CDX-1140 was specifically designed to balance systemic dosing and safety, which has proven elusive for CD40-targeted activating therapeutics," said Tibor Keler, Ph.D., Executive Vice President and Chief Scientific Officer of Celldex Therapeutics. "We have completed four of the potential eight monotherapy dose levels and, to date, CDX-1140 has been well tolerated. Importantly, we are observing dose-dependent biological effects consistent with CD40-mediated immune cell activity. Based on these positive findings, we have expanded development of the program and recently initiated a combination cohort with CDX-301, our dendritic cell growth factor, to increase the number of dendritic cells which are critical to initiating antitumor immunity and a key target for CDX-1140. We also expanded the study to include patients with non-Hodgkin’s lymphoma as our preclinical work has demonstrated that CDX-1140 has direct killing effect on CD40-expressing NHL cells. We look forward to continued data updates from this study in the first half of 2019."

Potent CD40 agonist antibodies have shown encouraging results in early clinical studies; however, systemic toxicity associated with broad CD40 activation has limited their dosing. CDX-1140 has unique properties relative to other CD40 agonist antibodies: potent agonist activity resulting in dendritic cell and B cell activation is independent of Fc receptor interaction, contributing to more consistent, controlled immune activation; CD40 ligand (CD154) binding is not blocked, allowing potential synergistic, antigen-specific agonist activity; and the antibody promotes strong immune activation without significant adverse events in preclinical toxicology studies.

Study Highlights:
Seventeen patients with solid tumors were enrolled at the time of data analysis (n=13 monotherapy; n=4 combination). Four single-agent dosing cohorts have completed (0.01; 0.03, 0.09 and 0.18 mg/kg) and enrollment to the 0.36 mg/kg monotherapy cohort is ongoing. Enrollment to the first CDX-1140/CDX-301 combination cohort is ongoing (0.09 mg/kg and 75 ug/kg, respectively). Dose dependent biological effects consistent with CD40-mediated immune activation have been observed in the study and no maximum tolerated dose (MTD) has been identified to date. Continued enrollment is ongoing to define the MTD and select a dose for disease-specific expansion cohorts that will be monitored for clinical activity.

CDX-1140 has been well tolerated to date. One patient experienced a grade 3 dose-limiting toxicity (DLT) (pneumonitis and hypoxia) at the single-agent 0.18 mg/kg dose. Per protocol, three additional patients were enrolled in the cohort and no additional DLTs have been observed in this or subsequent cohorts.

There have been no significant drug-related changes observed to date in liver function tests or platelets, which have been observed with other CD40 agonists.

Transient dose-dependent pharmacodynamic effects have been observed including activation of immune cells and increases in pro-inflammatory cytokines and chemokines in the blood, which are consistent with CD40-mediated immune activation and the hypothesis that CDX-1140 may achieve dose levels optimal for systemic exposure.
A combination cohort with Celldex’s dendritic cell growth factor CDX-301 has been added to the CDX-1140 study. Dendritic cells, which express CD40, are rarely present or completely absent within the tumor microenvironment and are critical for initiating anti-tumor immunity. CDX-301 is being utilized to increase the number of dendritic cells in blood and tissue available for CDX-1140 activation. CDX-1140 should, in turn, activate the dendritic cells, an important step for enhancing anti-tumor immune responses. While this combination cohort just recently opened to enrollment, preliminary evidence of enhanced immune activation has been observed. Patients continue to be monitored for toxicity with no DLT observed to date.
The study has also been amended to allow for the inclusion of patients with CD40-expressing B cell lymphomas (subtypes of non-Hodgkin lymphoma or NHL) in up to two single-agent cohorts. Both immune activation and direct killing of CD40-expressing NHL cells by CDX-1140 have been shown to contribute to antitumor activity. Several B cell lymphomas, including diffuse large B-cell lymphoma and follicular lymphoma, also express both CD40 and CD27. Celldex’s varlilumab is a potent CD27 agonist and has been shown to synergize with CDX-1140 in NHL models and may be evaluated in combination with CDX-1140 in the future.
About CDX-1140
CDX-1140 is a fully human antibody targeted to CD40, a key activator of immune response that is found on dendritic cells, macrophages and B cells and is also expressed on many cancer cells. Potent CD40 agonist antibodies have shown encouraging results in early clinical studies; however, systemic toxicity associated with broad CD40 activation has limited their dosing. CDX-1140 has unique properties relative to other CD40 agonist antibodies: potent agonist activity resulting in dendritic cell and B cell activation is independent of Fc receptor interaction, contributing to more consistent, controlled immune activation; CD40 ligand (CD154) binding is not blocked, allowing potential synergistic, antigen-specific agonist activity; and the antibody promotes strong immune activation without significant adverse events in preclinical toxicology studies. CDX-1140 has also shown direct antitumor activity in preclinical lymphoma models. Celldex believes that the potential for CDX-1140 will be best defined in combination studies with other immunotherapies, including CDX-301, Celldex’s dendritic cell growth factor, varlilumab, Celldex’s potent CD27 agonist, checkpoint blockade, radiation and other conventional cancer treatments.

On November 9, 2018 Asterias Biotherapeutics, Inc. (NYSE American: AST), a biotechnology company dedicated to developing cell-based therapeutics to treat neurological conditions associated with demyelination and cellular immunotherapies to treat cancer, reported financial and operational results for the third quarter ended September 30, 2018 (Press release, Asterias Biotherapeutics, NOV 9, 2018, View Source [SID1234531180]).

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On November 7, 2018, Asterias entered into a merger agreement under which Asterias will become a wholly-owned subsidiary of BioTime, Inc. (NYSE American and TASE: BTX) and each outstanding share of common stock of Asterias not already owned by BioTime will be converted into 0.71 common shares of BioTime. The transaction is expected to close during the Company’s first quarter ending March 31, 2019, subject to the satisfaction of customary closing conditions.

Third Quarter 2018 Financial Results

Research and development expenses were $3.5 million in the third quarter. General and administrative expenses were $1.9 million in the third quarter. Total operating expenses were $5.4 million in the third quarter of 2018, compared to $8.7 million in the third quarter of 2017.

Net loss was $4.5 million, or $0.08 per share for the third quarter of 2018 compared to a net loss of $6.8 million, or $0.14 per share for the third quarter of 2017. For the quarter ended September 30, 2018, net cash used in operating activities was $2.9 million compared to $4.5 million for the quarter ended September 30, 2017.

On September 28, 2018, the Company entered into two new agreements with an affiliate of Novo Nordisk, a multinational pharmaceutical company based in Denmark, which included a $2.0 million upfront payment that was received in early October 2018. Following the receipt of such funds from the Novo transaction, on October 1, 2018 the Company had cash and cash equivalents of $8.5 million and $6.2 in marketable equity securities. The Novo transaction will also result in approximately $1.0 million of annual reduction in fixed overhead allowing Asterias to advance its development programs more cost-effectively.

Conference Call

As a result of the merger agreement with BioTime, the Company’s previously announced conference to provide an overview of the third quarter results as well as the recent corporate progress, scheduled for Monday, November 12, 2018 at 5:00pm ET have been cancelled.

On November 9, 2018 Alligator Bioscience (Nasdaq Stockholm: ATORX), a biotechnology company that develops antibody-based drug candidates for tumor-directed immunotherapy and Aptevo Therapeutics Inc. (Nasdaq: APVO), a biotechnology company that develops new treatments in immunology and hematology, reported that new preclinical data for ALG.APV-527 will be presented at the 33rd Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) Scientific Conference, held in Washington, DC, USA, November 9-11, 2018 (Press release, Alligator Bioscience, NOV 9, 2018, View Source [SID1234531196]).

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ALG.APV-527 is a drug candidate for immunotherapeutic treatment of 5T4 positive solid cancer tumors. It is designed to activate the immune system via the co-stimulating receptor 4-1BB (CD137) on activated cytotoxic T cells and NK (Natural Killer) cells. ALG. APV-527 is designed to induce a powerful and tumor-directed immunoreactivation in the presence of 5T4 positive tumor cells. 5T4 is a tumor antigen found in a variety of malignant tumor types.

Preclinical data show that ALG.APV-527 is located in 5T4 positive tumors and selectively stimulates and enhances tumor-responsive immune responses of T cells and NKs, providing powerful anti-tumor effects. In brief, the preclinical data shows that ALG.APV-527 in the presence of 5T4 positive cells:

Increases the ability of CD8 positive T cells to secrete pro-inflammatory cytokines such as IFN gamma
Strengthens NK cell’s cell killability
In addition, the new data confirm that the 5T4 antigen is found in a variety of tumor types. 5T4 positive tumor cells were detected in non-small cell lung cancer (NSCLC) tumor, head and neck cancer, mesothelioma, pancreatic, bladder, kidney and ovarian cancer, but not in normal tissue samples such as liver and heart.

"Recent preclinical results further enhance ALG.APV-527’s potential for targeting 5T4 positive tumors and selectively activating the immune system via tumor-specific activation of T cells and NK cells. Overall, this gives potential for better anti-tumor effect with less side effects. We are now compiling a preclinical data packet with the goal of submitting a clinical trial (CTA) clinical trial in the second half of 2019, "said Christina Furebring, Senior Vice President Research at Alligator.

"Our new bispecific drug candidate ALG.APV-527 continues to show promising results in preclinical in vitro and in vivo studies. It exhibits properties such as goal-directed T-cell activation, optimized stability, an antibody-like half-life of 9 days, and good production characteristics. Aptevo and Alligator believe that this gives ALG.APV-527 a potential to become a unique anti-cancer drug for the treatment of several 5T4 expressive solid tumors, where there is today a major medical need. We are looking forward to submitting a CTA next year and then commencing clinical studies, "said Jane Gross, Chief Scientific Officer at Aptevo.

Alligator / Aptevos poster presentation titled "Potent Tumor-Directed T Cell Activation and Tumor Inhibition Induced by a 4-1BB x 5T4 ADAPTIR Bispecific Antibody " will be presented today November 9th from 18.45 to 14.45 (12.45-14.45 local) time) and from kl.30.30 to 2.30 (18.30-20.30 local time).

For more information, see View Source .

For further information please contact:
Cecilia Hofvander, Director Investor Relations & Communications
Telephone: 046-286 44 95
Email: [email protected]

This information is the information that Alligator Bioscience AB (publ) is obliged to disclose under the EU Market Abuse Regulation and the Securities Market Act. The information was provided, through the contact of the above contact person, for publication on November 9, 2018, at 06:00.

About ALG.APV-527
ALG.APV-527 is a bispecific antibody (4-1BB x 5T4) intended for tumor directed treatment of solid cancer tumors. ALG.APV-527 was constructed by combining Alligator’s antibody library ALLIGATOR-GOLD and Aptevo’s bispecific technology ADAPTIR . The antibody ALG.APV-527 consists of two parts, one activating tumor-specific T cells via the co-stimulating receptor 4-1BB (CD137) and the other binding to the protein 5T4 on the surface of tumor cells. This controls the immune activating effect of ALG.APV-527 to the tumor and not to normal tissue.

On November 9, 2018 Nektar Therapeutics (Nasdaq: NKTR) reported a presentation of new clinical and preclinical data for its I-O pipeline at the 2018 Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting (Press release, Nektar Therapeutics, NOV 9, 2018, View Source [SID1234531214]).

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New clinical study results from the PIVOT-02 Phase 1/2 Study were shared in an oral presentation titled, "Immune monitoring after NKTR-214 plus nivolumab (PIVOT-02) in previously untreated patients with metastatic Stage IV melanoma" (Abstract #O4) by Adi Diab, MD, Assistant Professor, Department of Melanoma Medical Oncology, Division of Cancer Medicine, University of Texas MD Anderson Cancer Center during the Cytokines Reinvented Session on Friday, November 9th.

Additional preclinical data presented at the annual meeting showed that NKTR-214 may drive, sustain and expand anti-tumor response when combined with therapies with complementary mechanisms of action including NKTR-262, poly (ADP-ribose) polymerase (PARP) inhibitors, radiation therapy (RT) and other agents. When combined with these treatments, NKTR-214 showed the potential to lead to tumor clearance and tumor specific immunologic memory.

"The data presented at this year’s SITC (Free SITC Whitepaper) Annual Meeting showcase our pipeline of novel investigational I-O agents that target key components of the immune cycle in order to restore immune surveillance and harness the body’s immune system to fight cancer," said Jonathan Zalevsky, Ph.D., Senior Vice President and Chief Scientific Officer at Nektar Therapeutics. "Clinical data presented for NKTR-214 show that NKTR-214 plus nivolumab give deep and durable responses in first-line IO-naive Stage IV melanoma patients, including a high rate of complete responses. For our TLR agonist candidate, NKTR-262, we presented data demonstrating alteration of the tumor micro-environment, including activating the innate and adaptive arms of the immune system along with encouraging anti-tumor activity."

Highlights from the oral presentation on Stage IV 1L Melanoma patients include:

Clinical Efficacy (Response measured per RECIST 1.1 by central independent radiology review for efficacy-evaluable patients treated at the recommended Phase 2 dose and with >1 on treatment scan). Response and median time on study calculated from data cut as of October 1, 2018:

Confirmed best overall response rate (ORR) was 53% (20/38) in efficacy-evaluable patients, with a 24% (9/38) complete response (CR) rate. Median time of follow-up was 7.2 months and median time to response was 2 months. 85% (17/20) patients with responses have ongoing responses. DCR, also known as disease control rate (CR+ PR + SD) was 76%.
Amongst the 33 patients with known pre-treatment PD-L1 status, ORR in PD-L1 negative patients was 6/14 (43%) and in PD-L1 positive patients was 13/19 (68%). One patient with unknown PD-L1 baseline status experienced a CR.
Clinical Safety (1L Melanoma safety database as of October 1, 2018):

A total of 41 patients have been treated at the RP2D. The most common (>30%) treatment-related adverse events (TRAEs) were grade 1-2 flu-like symptoms (78%), rash (70.7%), fatigue (63.4%), pruritus (46.3%), nausea (43.9%), arthralgia (36.6%) and myalgia (31.7%). A total of 8/41 (19.5%) of patients experienced a Grade 3 (G3) or higher TRAE with 2/41 (4.9%) patients discontinuing treatment due to a TRAE. 2/41 (4.9%) of patients experienced a G3 or higher immune-mediated AE.
A decreased frequency of Grade 1-2 cytokine related AEs was observed with continuous dosing.
Biomarkers and Mechanism of Action:

Clear activation of the IL-2 pathway demonstrated by an increase in absolute lymphocyte count with activated and proliferating CD4, CD8 and NK cells in blood.
Combination demonstrated T cell infiltration and activation in the tumor microenvironment.
TCR repertoire analysis demonstrates the presence of newly trafficked clonal infiltrates after treatment with NKTR-214 plus nivolumab.
Opdivo is a programmed death-1 (PD-1) immune checkpoint inhibitor that is designed to uniquely harness the body’s own immune system to help restore anti-tumor immune response. By harnessing the body’s own immune system to fight cancer, Opdivo has become an important treatment option across multiple cancers. NKTR-214 is an investigational immuno-stimulatory therapy designed to expand and activate specific cancer-fighting T cells and natural killer (NK) cells directly in the tumor micro-environment and increase expression of cell-surface PD-1 on these immune cells. A Phase 3 trial evaluating NKTR-214 in combination with nivolumab versus nivolumab in first-line advanced melanoma patients is currently recruiting patients (NCT03635983).

A copy of Dr. Diab’s presentation of PIVOT-02 data is available on Nektar’s corporate website at View Source

Details of the preclinical poster presentations at SITC (Free SITC Whitepaper) are as follows and each will be available for download at the time of presentation at View Source

Poster/Abstract #P364: "Systemic anti-tumor immunity and immune memory formation by a novel TLR7/8 targeting agent NKTR-262 combined with CD122-biased immunostimulatory cytokine NKTR-214", Kivimae, S., et al.

NKTR-262 and NKTR-214 in combination showed efficacy in all tested preclinical tumor models, correlated with sustained systemic expansion of tumor antigen specific CD8+ T cells.
Combining NKTR-262 with NKTR-214 coordinates tumor antigen presentation and costimulatory signaling with tumor antigen recognizing CD8+ T cell expansion to produce a sustained systemic anti-tumor immune response.
Poster/Abstract #P378: "NKTR-214 (CD122-biased agonist) and NKTR-262 (TLR7/8 agonist) combination treatment pairs local innate immune activation with systemic CD8+ T cell expansion to enhance anti-tumor immunity", Rolig, A., et al.

NKTR-214 and NKTR-262 resulted in systemic CD8+ T cell expansion, enhanced intratumoral CD8+ T cell effector function, and favorable myeloid polarization.
This robust anti-tumor immunity resulted in improved tumor regression and tumor-free survival in preclinical models.
Poster/Abstract #P368: "Combination of a Dipeptidyl Peptidase Inhibitor BXCL701 and Biased CD122 Agonist NKTR-214 with Anti-PD1 Provides Functional Immunological Memory through Inflammatory Cell Death", MacDougall, J., et al.

In a triple combination with NKTR-214 and an anti-PD-1 antibody, BXCL701 generated complete and durable responses in models with high densities of tumor associated. macrophages, validating the importance of engaging multiple cell types of the immune system required for complete anti-tumor response.
Poster/Abstract #P348: "Survival and immune modulation in homologous recombination deficient murine ovarian tumors using the PARP inhibitor, rucaparib and immune agonist, NKTR-214", Charych, D., et al.

NKTR-214 paired with rucaparib provided significantly increased survival and durable complete response than either treatment alone in murine models of ovarian cancer.
Preclinical results suggest the activity of this combination is through antigen priming of infiltrating memory T cells, increased NK cell recruitment and enhanced cytotoxicity of tumor infiltrates.
Poster/Abstract #P418: "Pre-clinical investigation of NKTR-255, a polymer-conjugated IL-15 with a potent NK cell dependent anti-tumor efficacy", Miyazaki, T., et al.

NKTR-255 demonstrated powerful immune stimulation of NK cells with dose-dependent effect in the proliferation and activation of NK cells and enhanced anti-metastatic activity in mouse lung metastasis models.
Results suggest NKTR-255 has high promise as a novel anti-tumor agent that boosts NK cell expansion and survival.
Poster/Abstract #P419: "NKTR-214 in combination with radiation produces a potent in situ vaccine in the syngeneic B78 melanoma model", Sondel, P., et al.

In a murine melanoma model study, the combination of NKTR-214 and radiation therapy (RT) resulted in significant tumor regression, higher rates of complete response, and stronger immunologic memory compared with radiation RT, RT plus IL-2, or NKTR-214 alone.
Poster/Abstract #P422: "A polymer-associated human IL-15 (NKTR-255) has optimized biological activity and unique mechanisms of action on CD8 T Cells and NK Cells", Robinson T., et al.

Preclinical findings highlighted the ability of NKTR-255 to impact different mechanisms of action on CD8 T cells and NK cells leading to novel therapeutic effects.
Poster/Abstract #P424: "NKTR-214, an engineered IL-2, selectively depletes intratumoral Tregs and expands immunotherapy-induced effector T cell responses", Sharma, M., et al.

NKTR-214 showed synergy with both checkpoint blockade and peptide-vaccination resulting in improved overall survival and cure of mice in models of colon carcinoma and melanoma.
The synergistic mechanism led to proliferation and tumor infiltration of effector CD8+ T cells while promoting selective intratumoral depletion of Tregs to establish effective anti-tumor immunity.
Poster/Abstract #P557: "Overcoming genetically-based resistance mechanisms to PD-1 blockade", Torrejón, D., et al.
[NOTE: These data were also presented in an oral presentation titled "Overcoming genetically-based resistance mechanisms to PD-1 blockade" by Davis Torrejón, M.D., UCLA Hematology-Oncology, during the Rapid Oral Abstract Presentations Session on Friday, November 9th.]

Genetic models of resistance to anti-PD-1 therapy were assessed using JAK1, JAK2, and B2M knockout (KO) models.
NKTR-214 overcame resistance to anti-PD-1 in the B2M-KO tumor model and significantly increased survival.
Analyst Call with Melanoma Specialists
Nektar will webcast an analyst and investor conference call with melanoma specialists and company management on Saturday, November 10, 2018 at 9:00 a.m. EST in Washington, D.C. during the 2018 Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting. The event follows today’s oral presentation of new efficacy, safety and immune monitoring data from the first-line Stage IV metastatic melanoma patient cohort in the PIVOT-02 study of NKTR-214 in combination with nivolumab.

Date and Time: Saturday, November 10, 2018 at 9:00 a.m. EST
Dial- in: 877-881-2183 (toll-free) or 970-315-0453 (enter access code 7865989)

Clinical investigators on the conference call will include Dr. Harriet Kluger, Professor of Medicine, Medical Oncology at the Yale Cancer Center and Dr. Adi Diab, Assistant Professor, Melanoma Medical Oncology at the University of Texas MD Anderson Cancer Center. Investors and analysts can also view slides and listen to the live audio webcast of the presentation at View Source The event will also be available for replay for two weeks on the company’s website, www.nektar.com.

About NKTR-214
NKTR-214 is a CD122-biased agonist designed to stimulate the patient’s own immune system to fight cancer. NKTR-214 is designed to grow specific cancer-killing T cells and natural killer (NK) cell populations in the body which fight cancer, which are known as endogenous tumor-infiltrating lymphocytes (TILs). NKTR-214 stimulates these cancer-killing immune cells in the body by targeting CD122 specific receptors found on the surface of these immune cells, known as CD8+ effector T cells and Natural Killer (NK) cells. CD122, which is also known as the Interleukin-2 receptor beta subunit, is a key signaling receptor that is known to increase proliferation of these effector T cells.1 In clinical and preclinical studies, treatment with NKTR-214 resulted in expansion of these cells and mobilization into the tumor micro-environment.2,3 NKTR-214 has an antibody-like dosing regimen similar to the existing checkpoint inhibitor class of approved medicines.

About NKTR-262
Cancer treatments that couple pharmacological activation of tumor antigen presentation with activation and expansion of CD8+ T and natural killer (NK) cells in the tumor environment have the potential to induce an effective anti-tumor immune response in patients. NKTR-262 is a novel small molecule agonist designed to activate toll-like receptors (TLRs). Intratumoral delivery of NKTR-262 promotes TLR activation to induce the development of antigen-specific immunity by initiating the process by which the immune system generates antigen-specific cytotoxic T cells to the patient’s specific tumor.4 NKTR-214 targets CD122 specific receptors found on the surface of these cancer-killing immune cells, known as CD8+ effector T cells. By first generating antigen-specific cytotoxic T cells with NKTR-262 and then growing these CD8+ effector T cells with NKTR-214, the patient’s entire immunity cycle can potentially be engaged to fight cancer. In preclinical studies, a single intratumoral dose of NKTR-262, administered in combination with NKTR-214, resulted in complete abscopal tumor regressions in multiple mouse syngeneic tumor models.5

About NKTR-255
NKTR-255 is a memory T cell stimulating cytokine designed to engage the IL-15 pathway to induce long-term T cell activation and improve the quality of T cell memory response to treat cancer. Through optimal engagement of the IL-15Rα/IL-2Rγ receptor complex, NKTR-255 stimulates proliferation and survival of CD8+ T cells, natural killer (NK) cells and enhances formation of long-term immunological memory which may lead to sustained anti-tumor immune response. Native rhIL-15 is rapidly cleared from the body and must be administered frequently and in high doses limiting its utility due to toxicity. NKTR-255 is designed with IL-15 receptor alpha specificity to optimize biological activity and is uniquely engineered to provide optimal exposure and an improved safety profile.

On November 9, 2019 CRISPR Therapeutics (NASDAQ:CRSP) and MaxCyte reported the expansion of their existing relationship by entering into a non-exclusive commercial license agreement that will allow CRISPR Therapeutics to deploy MaxCyte’s Flow Electroporation Technology to develop CRISPR/Cas9-based therapies in immuno-oncology (Press release, MaxCyte, NOV 9, 2018, View Source [SID1234537624]).

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"As we advance our allogeneic CAR-T programs into the clinic, we are preparing for the future by securing our access to the leading ex vivo delivery platform for both clinical and commercial use, just as we previously did for our hemoglobinopathy developmental candidates," said Samarth Kulkarni, CEO of CRISPR Therapeutics.

The expanded relationship builds on an existing agreement announced in March 2017 which allowed for the development of commercial therapeutics for hemoglobin-related diseases. Under the terms of the new license agreement, CRISPR Therapeutics will obtain non-exclusive development and commercial-use rights to MaxCyte’s cell engineering platform to develop immuno-oncology cell therapies. MaxCyte will supply its technology to CRISPR Therapeutics as part of the enabling technology license agreement and will receive milestone and sales-based payments in addition to other licensing fees.

"The expansion of our relationship with CRISPR Therapeutics signifies a key milestone for MaxCyte and our technology, providing further validation for the value and versatility of our technology as a leading enabler of next-generation cell-based therapies," said Doug Doerfler, President & CEO of MaxCyte, Inc. "CRISPR Therapeutics is a leader in gene editing, and we are very pleased to expand our collaboration into new therapeutic areas as we continue to explore the use of our technology to advance medicines to market that will make a difference for patients."

MaxCyte’s Flow Electroporation Technology enables the engineering of a broad range of therapeutically-relevant cell types at high efficiency while maintaining high viability and recovery. CRISPR Therapeutics’ immuno-oncology cell therapy programs rely on ex vivo gene editing, where the CRISPR components are delivered into T-cells using the MaxCyte technology.