On November 9, 2021 HotSpot Therapeutics, Inc., a biotechnology company pioneering the discovery and development of first-in-class allosteric therapies targeting regulatory sites on proteins referred to as "natural hotspots," reported new data validating its Smart Allostery platform in the elucidation and preclinical evaluation of a novel allosteric inhibitor of the E3 ubiquitin ligase CBL-B (Press release, HotSpot Therapeutics, NOV 9, 2021, View Source [SID1234594926]). The data will be presented at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 36th Annual Meeting, which is being held from November 10-14, 2021.

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"CBL-B’s role as a master negative regulator of T cells and NK cells makes it a very attractive target for cancer immunotherapy, but it has proven difficult to inhibit with traditional small molecules," said Geraldine Harriman, Ph.D., Co-Founder and Chief Scientific Officer at HotSpot Therapeutics. "We’re thrilled to share these new data showing that we can successfully inhibit CBL-B with a novel allosteric inhibitor identified through our Smart Allostery platform and promote T cell responses in vitro and in mice. To better treat patients, we need new mechanisms to enhance and sustain effective anti-tumor immunity and to address suboptimal responses. Our small molecule allosteric inhibitor of CBL-B may bring such benefit with the added advantage of convenient oral delivery."

CBL-B sits at a pivotal node in immune cell activation, and its inhibition holds the potential to address several key mechanisms where translational data supports a causative role in suboptimal response to current immunotherapies. Because inhibition of CBL-B lowers the threshold for T cell and NK cell activation, even in the absence of co-stimulatory signals, it may bring benefit to patients with low antigen levels (e.g., low TMB), low inflammation (e.g., low PDL-1) and/or sub-par co-stimulation (e.g., low CD28).

HotSpot’s Smart Allostery approach offers a diversity of advantages in delivering highly selective and differentiated orally bioavailable medicines against proteins that are undruggable or poorly druggable targets, including CBL-B. The platform utilizes a suite of computational algorithms powered by machine learning to uncover natural hotspots that control protein function, employs an array of specialized assays to identify hotspot binders and subsequently uses chemistry to selectively drug these sites with allosteric inhibitors.

SITC Presentation Overview:

Title: Identification of A Novel Allosteric Oral CBL-B Inhibitor that Augmented T Cell Response and Enhanced NK Cell Killing in vitro and in vivo
Authors: Jun Kuai, Yingzhi Bi, Yilin Qi, Deborah G Conrady, Rajiv G Govindaraj, Graham Hone, R. Aldrin Denny, Ken Carson, Geraldine Harriman, Fang Wang
Poster Number: 864
Session: Novel Single-Agent Immunotherapies

Summary of Poster

CBL-B is activated by tyrosine kinases and undergoes a large conformational change from closed inactive form to open active form.
Through the utilization of HotSpot’s proprietary Smart Allostery platform, including its AI-powered SpotFinder technology, a druggable phosphoregulatory pocket was identified in the inactive form of CBL-B.
HotSpot identified an inhibitor that binds to a regulatory hotspot on CBL-B, locking it in its inactive form, as confirmed by co-crystal structures.
This molecule prevents CBL-B phosphorylation, inhibits E3 ligase activity, promotes cytokine release, enhances T cell proliferation, and stimulates NK cell activation/killing.
In vivo, the molecule enhances T cells responses in anti-CD3 treated mice.

On November 9, 2021 Vigeo Therapeutics, a clinical-stage immuno-oncology company pioneering novel cancer therapies, reported new clinical data from its Phase 1/2 expansion study evaluating the single-agent activity of VT1021 in subjects with pancreatic cancer and recurrent glioblastoma (rGBM) (Press release, Vigeo Therapeutics, NOV 9, 2021, View Source [SID1234594925]). The data is being presented in the poster session at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) 2021 Annual Meeting, taking place from November 10-14, 2021.

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VT1021 is a first-in-class compound that induces the expression of Tsp-1 in the tumor microenvironment (TME). Tsp-1 then blocks the CD47 immune checkpoint and reprograms the CD36 receptor to induce tumor cell apoptosis, inhibit angiogenesis, and reprogram macrophages from the M2 to M1 phenotype. In the completed open-label, multicenter Phase 1/2 study (NCT03364400), the safety and preliminary anti-tumor efficacy of single-agent VT1021 was evaluated in subjects enrolled in both dose escalation and dose expansion cohorts. Results of the all-comer escalation cohort were presented at SITC (Free SITC Whitepaper) in 2020. In 2021, Vigeo is presenting the results of the expansion cohorts, which focused primarily on pancreatic cancer and rGBM, as well as other indications.

In the pancreatic cancer expansion cohort, VT1021, when administered as a single agent, was able to induce a reduction in tumor volume in 38% of subjects with measurable disease. VT1021 was able to reprogram the immune reactivity of the TME as evidenced by an increase in cytotoxic T lymphocytes (CTLs) as well as in the ratio of M1:M2 macrophages. These findings suggest that VT1021, in addition to its single agent activity, could be a potent and synergistic combination with checkpoint inhibitors.

Consistent with the reprogramming of the TME, Tsp-1 expression was significantly increased by VT1021 treatment across all tumor types. Induction of Tsp-1 protein was observed in circulating PBMCs, platelets and plasma, along with mRNA levels in PBMCs. Additionally, analysis of paired biopsy samples revealed increased Tsp-1 accumulation in MDSCs in the TME. Taken together these findings validate of the biological activity of VT021 via the induction of Tsp-1 in the TME.

"We are highly encouraged by the new data being presented at SITC (Free SITC Whitepaper), which demonstrate both a favorable safety profile for VT1021 as well as early signals of efficacy in pancreatic cancer – especially for those subjects with tumors expressing high levels of both CD47 and CD36," said CEO Jim Mahoney, "Out of 14 patients, 5 patients showed reduction in tumor burden. Based on these findings, we believe that VT1021, a dual-CD47/CD36 modulating agent, has strong potential as a treatment for pancreatic cancer patients."

Vigeo plans to initiate Phase 2/3 studies in both pancreatic cancer and rGBM during the first half of 2022. Vigeo will present additional results from the GBM expansion cohort at the Society for Neuro-Oncology (SNO) Conference in November 2021 in Boston, MA.

Details for the SITC (Free SITC Whitepaper) 2021 presentations are as follows:

Title: Clinical update of VT1021, a first-in-class CD36 and CD47 targeting immunomodulating agent, in subjects with pancreatic cancer and other solid tumors stratified by novel biomarkers
Presenter: Marsha Crochiere, PhD, Director of Translational Sciences, Vigeo Therapeutics
Session: Virtual Poster Hall
Poster #: 369
Date and time: A copy of the poster will be available on-demand starting Friday, November 12th at 7:00 AM ET

Title: Development of Thrombospondin-1 as a clinical pharmacodynamic biomarker for VT1021, a first-in-class therapeutic agent that reprograms the tumor microenvironment.
Presenter: Jian Jenny Chen, PhD, Director Scientific Research and Development, Vigeo Therapeutics
Session: Virtual Poster Hall
Poster #: 375
Date and time: A copy of the poster will be available on-demand starting Friday, November 12th at 7:00 AM ET

About VT1021
Vigeo’s lead asset, VT1021, is a first-in-class dual modulating compound that blocks the CD47 immune checkpoint and activates the apoptotic and macrophage reprogramming activity of CD36. The result of the dual modulating activity is the induction of apoptosis as well as an increase in both CTL:Treg and M1:M2 macrophage ratio. The biological/therapeutic activity of VT1021 is mediated by the stimulation of thrombospondin-1 (Tsp-1). Through these dual-modulating effects VT1021 reprograms the tumor microenvironment (TME) from one that is immune suppressive, or "cold," to immune enhanced (or sensitized), or "hot," that are more susceptible to attack from the immune system. Vigeo is developing VT1021 as a therapeutic agent across a range of cancers, with a current focus on solid tumors.

On November 9, 2021 I-Mab (Nasdaq: IMAB), a clinical-stage biopharmaceutical company committed to the discovery, development, and commercialization of novel biologics, and ABL Bio, Inc. (Kosdaq:298380, hereafter "ABL"), a clinical-stage biotech developing bispecific antibody technology for immune-oncology and neurodegenerative diseases, reported preclinical data of their 4-1BB bispecific antibodies at the 2021 Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting (Press release, I-Mab Biopharma, NOV 9, 2021, View Source [SID1234594924]). The new data demonstrate the unique mechanisms of action of TJ-CD4B/ABL111 and TJ-L14B/ABL503 which have resulted in localized drug action and reduced systemic toxicity, as well as sustained anti-tumor efficacy.

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Stimulation of 4-1BB is a promising therapeutic strategy for improving the current immunotherapy for multiple cancers. TJ-CD4B/ABL111 and TJ-L14B/ABL503, both jointly developed by I-Mab and ABL, are undergoing phase 1 clinical studies in the United States.

"Bispecific antibodies are rapidly recognized for their transformative potential, and our pipeline of highly-differentiated 4-1BB bispecific therapies are key components of our biologics pipeline development strategy," said Dr. Taylor Guo, Chief Scientific Officer of I-Mab. "Dose-limiting toxicities have hampered clinical development of 4-1BB targeting molecules as a drug class. The studies being presented at SITC (Free SITC Whitepaper) suggested that both our bispecific assets could have the ability to overcome this common problem, and we are confident that this differentiation places TJ-CD4B/ABL111 and TJ-L14B/ABL503 at the forefront of 4-1BB bispecific development."

"The preclinical data from this pair of bispecific molecules prove that our ‘Grabody-T’ platform effectively reduces peripheral toxicity by allowing the activation of T cells only in the tumor microenvironment," said Dr. Sang Hoon Lee, CEO of ABL Bio. "We look forward to further validating its therapeutic potential in the ongoing clinical studies and as we continue to develop 4-1BB bispecific antibodies in various cancer indications."

Key data highlights:

TJ-CD4B/ABL111

Poster title (#702): TJ-CD4B (ABL111), a Claudin18.2-targeted 4-1BB tumor engager induces potent tumor-dependent immune response without dose-limiting toxicity in preclinical studies

The preclinical studies confirmed the unique pharmacodynamic data and safety of TJ-CD4B/ABL111 in animal models and cell cultures. Analysis of the data found:

Potent, anti-tumor activity was observed with the proliferation of immune cells in the tumor microenvironment (TME) as well as an increase in memory T cells in the peripheral blood, suggesting long-term immunity against the tumor.
TJ-CD4B/ABL111 was well tolerated in non-human primates and did not induce a systemic immune response or liver toxicity up to levels of 100mg/kg.
Activation of immune pathways by TJ-CD4B/ABL111 was demonstrated by a pro-inflammatory profile and increased gamma interferon-regulated gene expression in primary human CD8+ T cells co-cultured with CLDN18.2 expressing cells.
TJ-L14B/ABL503

Poster title (#892): ABL503 (TJ-L14B), PD-L1x4-1BB bispecific antibody induces superior anti-tumor activity by PD-L1-dependent 4-1BB activation with the increase of 4-1BB+CD8+ T cells in tumor microenvironment

The preclinical study data confirms the unique mechanism of action of TJ-L14B/ABL503 and its potential to treat resistance to PD-L1 therapies. Analysis of the data found:

PD-L1-dependent stimulation of the 4-1BB signaling pathway was demonstrated in 4-1BB bioassays with PD-L1 expressing tumor cells
More potent 4-1BB activation by TJ-L14B/ABL503 was observed at higher PD-L1 expression confirming the requirement of PD-L1 on both tumor and immune cells for optimal activity. Cytokine release assays have also demonstrated minimal peripheral toxicity with TJ-L14B/ABL503
The in vivo efficacy of TJ-L14B/ABL503 was demonstrated in animal models with tumors expressing different levels of PD-L1. TJ-L14B/ABL503 showed anti-tumor efficacy across the PD-L1 levels. In particular, TJ-L14B/ABL503 demonstrated superior anti-tumor efficacy than atezolizumab in tumors with low PD-L1 expression
In vitro tumor-killing activity of TJ-L14B/ABL503 was superior compared to atezolizumab when tested in organoid system, even in organoids from atezolizumab non-responders
Pharmacodynamic changes in TILs and blood were evaluated in animal models. An increase in 4-1BB+ cells, CD8+ T cells, and effector memory T cells was observed in the TME and blood, indicating a strong and long-lasting anti-tumor immune response
Treatment with TJ-L14B/ABL503 increased MIG/CXCL9, MIP-1b/CCL4, and s4-1BB in the serum, and can potentially be used as pharmacodynamic markers in clinical trials
About TJ-CD4B/ABL111

TJ-CD4B, also known as ABL111, is a Claudin 18.2 and 4-1BB bispecific antibody capable of binding to tumor cells expressing Claudin 18.2, i.e., gastric cancer and pancreatic cancer cells, and stimulating intra-tumoral T cells by the 4-1BB arm designed to be activated only upon tumor engagement while silent elsewhere. TJ-CD4B/ABL111 effectively maintains a strong tumor binding property and anti-tumor activity attributable to a synergistic effect of both Claudin 18.2 antibody and 4-1BB antibody while it avoids or minimizes liver toxicity and systemic immunotoxicity commonly seen with 4-1BB antibodies as a drug class. Being developed under collaboration between I-Mab and ABL, TJ-CD4B/ABL111 is currently being investigated in a phase 1 clinical study in the U.S.

About TJ-L14B/ABL503

Being developed jointly with ABL, TJ-L14B/ABL503 is a differentiated PD-L1-based bispecific antibody with the PD-L1 arm as the tumor-dependent T-cell activator and the 4-1BB arm as the conditional T cell activator upon tumor engagement. Using ABL’s "Grabody-T" bispecific antibody platform technology, TJ-L14B/ABL503 stimulates 4-1BB activation only in the presence of PD-L1 expressing tumor cells to minimize the risk of off-tumor toxicity. Preclinical studies have demonstrated that the bispecific antibody shows better anti-tumor activity than equimolar doses of single agents alone or in combination. Phase 1 study in currently being conducted in the U.S.

On November 9, 2021Poseida Therapeutics, Inc. (Nasdaq: PSTX), a clinical-stage biopharmaceutical company utilizing proprietary genetic engineering platform technologies to create cell and gene therapeutics with the capacity to cure, reported the upcoming presentation of preclinical data highlighting P-BCMA-ALLO1 for the treatment of relapsed/refractory multiple myeloma and P-MUC1C-ALLO1 for the treatment of multiple solid tumor indications at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 2021 Annual Meeting (SITC) (Free SITC Whitepaper), being held in Washington, D.C., and virtually November 10-14, 2021 (Press release, Poseida Therapeutics, NOV 9, 2021, View Source [SID1234594923]).

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"We are pleased to share preclinical data for P-BCMA-ALLO1 and P-MUC1C-ALLO1, our first fully allogeneic candidates," said Devon Shedlock, Ph.D., Chief Scientific Officer, Cell Therapies at Poseida Therapeutics. "The results being shared at SITC (Free SITC Whitepaper) not only demonstrate potent antitumor efficacy in preclinical models for our allogeneic product candidates, but also further validate the capabilities of our piggyBac and Cas-CLOVER technologies. Using our proprietary manufacturing process which includes our booster molecule, we have the potential to produce hundreds of patient doses from a single manufacturing run while also preserving high levels of stem cell memory T cells (TSCM), which are correlated with antitumor efficacy in the clinic. We have recently received FDA clearance on our P-BCMA-ALLO1 IND and are in the process of initiating a Phase 1 trial. We look forward to advancing our P-MUC1C-ALLO1 CAR-T candidate with an IND filing expected later this year."

Poseida is presenting two posters, which will be on display on the SITC (Free SITC Whitepaper) 2021 virtual meeting platform from 7 a.m. EST on Friday, Nov. 12, 2021 until the virtual meeting platform is closed on Jan. 9, 2022.

Presentation Highlights:

In the poster titled "Memory Phenotype in Allogeneic Anti-BCMA CAR-T Cell Therapy (P-BCMA-ALLO1) Correlates with In Vivo Tumor Control" (Abstract Number 147), Hubert Tseng, Ph.D., Poseida Therapeutics, will highlight:

Using the Company’s piggyBac DNA Delivery System in combination with its Cas-CLOVER gene editing system and a proprietary "booster molecule," Poseida generated doses of P-BCMA-ALLO1 from healthy donor T cells and consistently maintain high frequency of stem cell memory T cells.
Cas-CLOVER was used to eliminate surface expression of both the TCR and MHC class I to make fully allogeneic CAR-T cells. In addition to the CAR molecule, piggyBac enables delivery of a selectable marker allowing the generation of a final cell product that is >95% CAR-positive.
P-BCMA-ALLO1 is comprised of a high frequency of TSCM. It has potent in vivo antitumor activity, which is comparable to non-edited autologous anti-BCMA CAR-T cell therapy. Expression of memory markers at both the mRNA and protein levels across individual lots significantly correlates with in vivo tumor control.
P-BCMA-ALLO1 is a highly potent and safe allogeneic anti-BCMA CAR with a manufacturing process that consistently maintains a TSCM phenotype, which correlates with antitumor efficacy. P-BCMA-ALLO1 has received FDA IND clearance and is advancing rapidly toward the clinic.
In the poster titled "P-MUC1C-ALLO1: A Fully Allogeneic Stem Cell Memory T Cell CAR-T Therapy with Broad Potential in Solid Tumor" (Abstract Number 123), Yan Zhang, Ph.D., Poseida Therapeutics, will highlight:

P-MUC1C-ALLO1 is manufactured using Poseida’s piggyBac DNA delivery system and Cas-CLOVER gene editing system to knockout both the TCR and MHC class I proteins. Poseida can generate significant doses of P-MUC1C-ALLO1 including a high-percentage of desirable TSCM cells.
P-MUC1C-ALLO1 displayed specificity for tumor vs normal cells: MUC1C CAR-T cells had potent cytotoxicity against tumor cells, and minimal killing of normal MUC1-C-positive human primary cells.
In a triple negative breast cancer xenograft model, P-MUC1C-ALLO1 eliminated established tumor cells, demonstrating robust T cell expansion in peripheral blood and maintained a favorable TSCM percentage over time.
P-MUC1C-ALLO1 has also shown robust efficacy in a peritoneal ovarian cancer xenograft model, eliminating established tumor cells to undetectable levels with minimal toxicity.
About P-BCMA-ALLO1
P-BCMA-ALLO1 is Poseida’s first fully allogeneic product candidate targeting B-cell maturation antigen (BCMA) for the treatment of relapsed/refractory multiple myeloma. In in vitro and in vivo preclinical studies, P-BCMA-ALLO1 showed effective targeted cancer cell killing and cytokine secretion, with similar or superior performance in anti-tumor efficacy compared to an autologous CAR-T therapy, P-BCMA-101. Inclusion of a proprietary booster molecule in the allogeneic manufacturing process further improves expansion of gene-edited cells and may potentially enable production of hundreds of patient doses from a single manufacturing run, thereby potentially reducing the manufacturing cost per dose into the same range as that of a monoclonal antibody. In August 2021, Poseida announced that its Investigational New Drug (IND) application for P-BCMA-ALLO1 received clearance from the U.S. Food and Drug Administration (FDA).

About P-MUC1C-ALLO1
P-MUC1C-ALLO1 is an allogeneic CAR-T product candidate in preclinical development with the potential to treat a wide range of solid tumors derived from epithelial cells, including breast and ovarian cancers, as well as other cancers expressing a cancer-specific form of the Mucin 1 protein, or MUC1C. We have designed P-MUC1C-ALLO1 to be fully allogeneic, with genetic edits to eliminate or reduce both host-vs-graft and graft-vs-host alloreactivity. We have demonstrated the elimination of tumor cells to undetectable levels in preclinical models of breast cancer and ovarian cancer.

On November 9, 2021 Nektar Therapeutics (NASDAQ:NKTR) reported that it will host a webcast analyst and investor conference call with a cancer specialist and Nektar management on Friday, November 12, 2021, at 12:00 p.m. EST during the 2021 Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) Annual Meeting (Press release, Nektar Therapeutics, NOV 9, 2021, https://www.prnewswire.com/news-releases/nektar-therapeutics-to-host-webcast-conference-call-for-analysts–investors-with-cancer-specialist-during-2021-society-for-immunotherapy-of-cancer-sitc-36th-annual-meeting-301419303.html [SID1234594922]). The call will be hosted by Nektar management and will include, SITC (Free SITC Whitepaper) author and presenter, Dr. Mehmet Altan, Assistant Professor, Department of Thoracic/Head and Neck Medical Oncology, Division of Cancer Medicine at The University of Texas Anderson Cancer Center and Dr. Alan Tan, Director of GU Medical Oncology and Assistant Professor in the Division of Hematology, Oncology and Cell Therapy at Rush University Medical Center.

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The event will follow the publication of the NKTR-255 poster (Abstract #957) on Friday morning. SITC (Free SITC Whitepaper) is being held in Washington, D.C. and virtually from November 10 to November 14, 2021.

Analyst Call:

Date and Time: Friday, November 12, 2021, at 12:00 p.m. EST

Dial-in: 877-881-2183 (toll-free) or 970-315-0453 (enter access code 1769208)

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 Nektar’s website: www.nektar.com.

Details of the presentations at SITC (Free SITC Whitepaper) are as follows:

Nektar Poster Presentations at SITC (Free SITC Whitepaper)

Abstract 957: "NKTR-255 Plus Cetuximab in Patients with Solid Tumors: Interim Safety and Efficacy Results from the Phase 1b Dose Escalation Study," Altan, M., et al.

Presenter: Dr. Mehmet Altan, MD Anderson Cancer Center
ePoster and live poster will be available on Friday, November 12th, 2021, at 7:00 a.m. EST
Poster reception: Friday, November 12, 2021, from 7:00 p.m. – 8:30 p.m. EST
Additional Collaborator Presentations at SITC (Free SITC Whitepaper)

Abstract 59: "Associations between KIR/KIR-ligand genotypes and clinical outcome for patients with advanced solid tumors receiving BEMPEG plus nivolumab combination therapy in the PIVOT-02 trial," Feils, AS., et al.

ePoster will be on display on the SITC (Free SITC Whitepaper) 2021 virtual meeting platform on Friday, November 12, 2021, at 7:00 a.m. EST
Abstract 596: "Combining Bempegaldesleukin (CD122-preferential IL-2 pathway agonist) and NKTR-262 (TLR7/8 agonist) pairs local innate activation with systemic CD8+ T cell expansion to enhance anti-tumor immunity," Rolig, A., et al.

ePoster will be on display on the SITC (Free SITC Whitepaper) 2021 virtual meeting platform on Friday, November 12, 2021, at 7:00 a.m. EST
Dr. Mehmet Altan

Mehmet Altan, MD, is an Assistant Professor in the Department of Thoracic/Head and Neck Medical Oncology, Division of Cancer Medicine at The University of Texas Anderson Cancer Center. Dr. Altan is one of the lead investigators in the phase 1/2, dose-escalation and dose-expansion study of NKTR-255 in combination with cetuximab in patients with refractory 2nd and 3rd line metastatic colorectal cancer or metastatic head and neck cancer. His current research areas include identification of mechanisms for primary and secondary resistance to immunotherapies and predictive markers for immunotherapy toxicities. He also works on translational research projects for identification of spatiotemporal dynamics of the tumor microenvironment in response to immunotherapy to define potential therapeutic targets.

Dr. Alan Tan

Alan Tan, MD, is a Director of GU Medical Oncology and an Assistant Professor in the Division of Hematology, Oncology and Cell Therapy at Rush University Medical Center. He specializes in kidney cancer, urothelial/bladder cancer, prostate cancer and melanoma. Dr. Tan has clinical research interest in designing and implementing clinical trials to test novel immunotherapies and targeted therapies in these cancers. He also leads the Rush University Precision Oncology and Genomics program. He is co-chair for the Hoosier Cancer Research Network (HCRN) Melanoma Working Group.