Celldex Presents Emerging MerTK Antibody Program at the Society for Immunotherapy of Cancer’s 33rd Annual Meeting

On November 10, 2018 Celldex Therapeutics, Inc. (NASDAQ:CLDX) reported data from the Company’s MerTK antibody program in a poster session at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) 33rd Annual Meeting(Press release, Celldex Therapeutics, NOV 10, 2018, View Source [SID1234531099]). MerTK is emerging as a promising target for cancer immunotherapy. Its expression in innate immune cells is believed to negatively regulate immune responses and genetic removal of MerTK renders mice resistant to some tumors.

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"MerTK has been described as an immune checkpoint in macrophages, dendritic cells and other immune cells," said Tibor Keler, Ph.D., Executive Vice President and Chief Scientific Officer of Celldex Therapeutics. "Through our significant discovery effort, we have identified two unique antibodies that modulate this pathway resulting in profound levels of cytokine and chemokine production, and importantly we have developed preclinical models that support the premise that antibody modulation of MerTK can lead to antitumor responses."

As detailed in the presentation, Celldex developed a large panel of antibodies to MerTK and investigated their ability to enhance activation of innate immune cells. Two lead candidate human anti-MerTK antibodies were then selected based on their potent induction of cytokines from human macrophages, dendritic cells, and monocytes. Treatment of dendritic cells with the MerTK antibodies led to production of a broad array of pro-inflammatory cytokines and chemokines. Isolated peripheral blood monocytes were found to express high levels of MerTK and were similarly activated by the MerTK antibodies.

Emerging proof of concept data was established in preclinical models. Using a surrogate anti-mouse MerTK​ antibody, similar increases in the levels of cytokines were observed in the blood of mice shortly after treatment with the antibody. The anti-mouse MerTK​ antibody led to increased survival when dosed alone or in combination with a PD-1 inhibitor in a colon cancer model. To test the lead clinical candidates, which bind to human and not mouse MerTK, Celldex generated human MerTK transgenic mice that were shown to appropriately express and regulate human MerTK on macrophages. This will now allow testing of the anti-human MerTK mAbs in inflammation and tumor models. Collectively, the data support that anti-MerTK mAbs can modulate MerTK activity consistent with its role as a negative immune regulator and provide an exciting new approach to enhance innate immune function in cancer.

Celldex is currently completing the preclinical studies for selection of the lead candidate to advance into development activities. These studies include investigating the antitumor effect of combinations with Celldex’s immunotherapy product candidates.

Infinity Reports Clinical and Translational Data from Expansion Cohorts of MARIO?1 Phase 1b Study of IPI-549 in Combination with Opdivo® (nivolumab) at SITC’s 33rd Annual Meeting

On November 10, 2018 Infinity Pharmaceuticals, Inc. (NASDAQ: INFI) reported that data to be presented today at the 33rd Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) demonstrated preliminary evidence that IPI-549 in combination with Opdivo (nivolumab) is clinically active in indications not expected to respond to Opdivo alone (Press release, Infinity Pharmaceuticals, NOV 10, 2018, View Source [SID1234531169]). In particular, evidence of reversal of resistance to Opdivo included a partial response in a patient with metastatic melanoma who progressed on immediate prior Opdivo therapy. IPI-549 plus Opdivo also resulted in a 26% reduction of tumor target lesions in a patient with chemotherapy-resistant triple negative breast cancer (TNBC), a tumor type intrinsically resistant to checkpoint inhibition. The data also included long-term follow up on sustained partial responses in two patients from combination dose escalation: one with microsatellite stable (MSS) gallbladder cancer and one with adrenocortical carcinoma. The observed early clinical activity from the combination expansion, in addition to findings from the monotherapy cohorts, including associated translational data, support on-mechanism proof of concept for IPI-549. The late-breaking abstract describing these findings will be presented today in a poster presentation at the SITC (Free SITC Whitepaper)’s 33rd Annual Meeting taking place in Washington, D.C., November 7 – 11, 2018.

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"There continues to be a significant need for improvement in the treatment of patients with advanced solid tumors who do not respond to checkpoint inhibitors alone. IPI-549’s potential to improve upon the existing CPIs makes it an important first-in-class drug in development," said David Hong, M.D. Deputy Chair, Department of Investigational Cancer Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX. "The reversal of resistance to checkpoint inhibition is particularly encouraging for the further development of IPI-549, and I look forward to my continued participation in the development of IPI-549."

Infinity is evaluating IPI-549 in MARIO-1, a Phase 1b study in approximately 200 patients with advanced solid tumors. Additionally, Infinity is planning to initiate MARIO-275, a global, randomized Phase 2 study to evaluate the effect of adding IPI-549 to Opdivo in approximately 150 checkpoint-inhibitor naïve advanced urothelial cancer patients who have progressed or recurred following treatment with platinum-based chemotherapy.

"The rigorous design of our Phase 1b study sets a high bar for the determination of proof of concept, given that the goals of our study are to see clinical activity both in settings where patients are not expected to respond to Opdivo alone, and in indications where there are high levels of immunosuppressive macrophages," said Dr. Sam Agresta, Chief Medical Officer of Infinity Pharmaceuticals. "We do this with the intention of re-sensitizing patients to Opdivo to overcome the limiting effects of macrophages to checkpoint inhibitor therapy, and we are excited that the data we shared today demonstrate clinical activity in this patient population. We look forward to the maturation of MARIO-1 and the advancement of the IPI-549 clinical development program in the checkpoint-inhibitor naïve setting with MARIO-275."

"Today’s data validate our scientific rationale for the development of IPI-549 as a potentially first-in-class therapeutic alternative for patients lacking better treatment options," said Adelene Perkins, Chief Executive Officer of Infinity Pharmaceuticals. "We will be expanding our melanoma cohort, with patients refractory to immediate prior anti-PD1 therapy, to 40 patients based on promising early signals and have triggered expansion of the TNBC cohort. We will also be initiating our Phase 2 MARIO‑275 trial in urothelial cancer with an emphasis on patients with high myeloid derived suppressor cell levels, given that MDSCs further promote immunosuppression. We look forward to providing an update on these efforts."

Details of Today’s Late-Breaking Presentation

Infinity will present a poster entitled "The first clinical/translational data from the expansion cohorts of a Ph1/1b Study of IPI-549, a tumor macrophage-reprogramming small molecule, in combination with nivolumab in advanced solid tumors" (Poster P716). The data reported today from an October 14, 2018 data cutoff included 82 patients treated with IPI-549 at 40 mg QD and Opdivo at 240mg IV once every two weeks.

Summary of Data

Combination expansion data demonstrated that IPI-549 in combination with Opdivo is well tolerated and is associated with a favorable safety profile. Among 82 patients evaluable for safety, the majority of side effects reported were Grade 1 or Grade 2, with 3 (4%) patients discontinuing the study due to treatment-related toxicities. There were no treatment-related deaths. These 82 patients have been treated in seven distinct cohorts: non-small cell lung cancer (n=8), melanoma (n=15), head and neck cancer (n=12), triple negative breast cancer (n=17), adrenocortical cancer (n=5), mesothelioma (n=11), and a biomarker defined baseline MDSC high cohort (n=14). The majority of the study population is 4th line and resistant to anti-PD1/PDL1 therapy. Among the 44 patients evaluable for activity (approximately one-third of the planned 129 patients in the combination expansion cohorts), 15 patients showed a best response of stable disease or better, including one partial response in an advanced melanoma patient who progressed on immediate prior Opdivo therapy. In addition, a patient with chemotherapy-resistant triple negative breast cancer showed 26% reduction in tumor target lesions at the first assessment. Reductions in elevated baseline levels of MDSCs as well as corresponding increases in the proliferative fraction of previously exhausted memory cytotoxic T-cells were seen in these patients. Another partial response was observed in a patient with advanced mesothelioma. Twenty-five patients remain on study and were not evaluable for activity as of the data cutoff. The data included long-term follow up on additional partial responses in two patients from the combination dose escalation: one with microsatellite stable gallbladder cancer and one with adrenocortical carcinoma and these two partial responses were maintained for over 12 and 17 months, respectively. These patients also demonstrated sustained inhibition of MDSCs during the period in which the partial response was maintained. Enrollment is ongoing.

Infinity Investor/Analyst Reception and Webcast
In conjunction with SITC (Free SITC Whitepaper)’s 33rd Annual Meeting, Infinity will host a reception and webcast for investors and analysts today, November 10, 2018, beginning at 6:30 a.m. ET to discuss the clinical development of IPI-549, including a review of data from the Phase 1b clinical study.

The event will feature David Hong, M.D., Deputy Chair, Department of Investigational Cancer Therapeutics, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX.

The webcast and accompanying slides can be accessed in the "investors/media" section of the company’s website, www.infi.com. A replay of the event will also be available.

About IPI-549 and the Ongoing MARIO-1 Phase 1/1b Study
IPI-549 is an investigational first-in-class, oral, immuno-oncology product candidate targeting tumor-associated myeloid cells through selective phosphoinositide-3-kinase-gamma (PI3K-gamma) inhibition, thereby reducing pro-tumor macrophage function and increasing anti-tumor macrophage function. In preclinical studies, IPI-549 demonstrated the ability to reprogram macrophages from a pro-tumor (M2), immune suppressive function, to an anti-tumor (M1) immune activating function and enhance the activity of, and overcome resistance to, checkpoint inhibitors.i ii As such, IPI-549 may have the potential to treat a broad range of solid tumors and represents a potentially additive or synergistic approach to restoring anti-tumor immunity in combination with other immunotherapies such as checkpoint inhibitors.

The ongoing Phase 1/1b study being conducted by Infinity is designed to evaluate the safety, tolerability, activity, pharmacokinetics and pharmacodynamics of IPI-549 as a monotherapy and in combination with nivolumab (Opdivo) in approximately 200 patients with advanced solid tumors.iii The study includes monotherapy and combination dose-escalation components, in addition to monotherapy expansion and combination expansion components. The monotherapy dose-escalation and expansion components are complete. The combination dose-escalation component is also complete, and combination expansion cohorts are enrolling.

The combination expansion component of the study includes multiple cohorts designed to evaluate IPI-549 in patients with specific types of cancer, including patients with non-small cell lung cancer, melanoma and head and neck cancer whose tumors show initial resistance or initially respond to but subsequently develop resistance to immune checkpoint blockade therapy. The combination expansion component also includes a cohort of patients with triple negative breast cancer who have not been previously treated with immune checkpoint blockade therapy, a cohort of patients with mesothelioma, a cohort of patients with adrenocortical carcinoma and a cohort of patients with high baseline blood levels of MDSCs.

About the Planned MARIO-275 Phase 2 Study
Infinity is planning to conduct MARIO-275: MAcrophage Reprogramming in Immuno-Oncology, a global, randomized Phase 2 study to evaluate the effect of adding IPI-549 to Opdivo in checkpoint-naïve advanced urothelial cancer patients who have progressed or recurred following treatment with platinum-based chemotherapy. Approximately 150 patients will be randomized between combination therapy and Opdivo monotherapy. The primary endpoint of the trial will be overall response rate, which will be assessed in the overall population as well as in subsets of patients with different baseline levels of myeloid derived suppressor cells (MDSCs). Opdivo is approved for use by the FDA as a single agent in patients with locally advanced or metastatic urothelial cancer who have progressed or recurred following treatment with platinum-based chemotherapy or who have disease progression within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy. In exploratory analyses of the CheckMate-275 data, high levels of MDSCs were associated with shorter overall survival in patients treated with Opdivo2. In Infinity’s MARIO-1study, MDSCs were reduced in the majority of patients treated with IPI-549 monotherapy.3 IPI-549 in combination with Opdivo has been administered to over 80 patients and demonstrated early evidence of clinical activity with translational studies demonstrating evidence of on-mechanism IPI-549-mediated effects.4

IPI-549 is an investigational compound, and its safety and efficacy has not been evaluated by the U.S. Food and Drug Administration or any other health authority.

Jounce Therapeutics Presents Reverse Translational, Biomarker and Preclinical Data from ICOS Program at the Society for Immunotherapy of Cancer’s (SITC) 33rd Annual Meeting

On November 10, 2018 Jounce Therapeutics, Inc. (NASDAQ: JNCE), a clinical-stage company focused on the discovery and development of novel cancer immunotherapies and predictive biomarkers, reported that reverse translational and biomarker data derived from its ICONIC (ICOS AgONist Antibody for Immunotherapy in Cancer Patients) trial of JTX-2011 and preclinical data from the ICOS (Inducible T cell CO-Stimulator) program were presented at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) 33rd Annual Meeting, being held November 9-11, 2018 in Washington, D.C (Press release, Jounce Therapeutics, NOV 10, 2018, View Source;p=RssLanding&cat=news&id=2376614 [SID1234531232]).

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"The data presented at SITC (Free SITC Whitepaper)’s 33rd Annual Meeting demonstrate the role of JTX-2011 in the emergence and agonism of ICOS hi CD4 T effector cells and provide further evidence in support of the biological and clinical activity of JTX-2011. The regimens we are advancing, including ongoing combinations with ipilimumab, are grounded in these important scientific findings," said Elizabeth Trehu, M.D., chief medical officer of Jounce Therapeutics. "New insights from our Translational Science Platform continue to inform JTX-2011 clinical development. We believe our science-based approach is necessary to develop new immunotherapies to benefit cancer patients."

Data presented from ICONIC patients demonstrate the agonistic properties of JTX-2011. These data are in addition to the subset analysis data presented at ASCO (Free ASCO Whitepaper) 2018 demonstrating the emergence of ICOS hi CD4 T cells in the bloodstream in all patients with ≥30% target lesion tumor reductions, both in patients treated with JTX-2011 monotherapy and in combination with nivolumab. The ICOS hi CD4 T cells were not observed in patients with primary progressive disease.

"Through additional reverse translational studies presented today, we established two key insights that provide the scientific foundation for the next stage of development of JTX-2011," said Richard Murray, Ph.D., chief executive officer and president of Jounce Therapeutics. "First, the emergence of these ICOS hi CD4 T cells was related to JTX-2011, as it has not been detected in a separate study we conducted of responding and non-responding patients that received PD-1/L1 inhibitor monotherapy treatment; and second, in vitro experimental data showed that JTX-2011 only activates CD4 T cells if they already express high levels of ICOS. Additionally, new preclinical tumor model data presented in a separate poster, strengthens our belief that agents that induce ICOS hi CD4 T cells detectable in the bloodstream, such as anti-CTLA-4, may be attractive combination partners for JTX-2011."

In a poster titled "Emergence of an ICOS hi CD4 T cell subset correlates with tumor reductions in subjects treated with the ICOS agonist antibody JTX-2011," Jounce researchers describe the reverse translational efforts ongoing in the ICONIC trial including:

Follow-up on the initial observation of the emergence of ICOS hi CD4 T cells. Emergence of this cell population, which correlated with clinical benefit in patients treated with both JTX-2011 monotherapy and in combination with nivolumab, was presented at ASCO (Free ASCO Whitepaper) in June 2018. These data build upon the initial observation and provides further characterization of the emerging cell population as T effector and not T regulatory cells and includes evidence that the cells do not emerge in patients responding to PD-1 monotherapy.
Additional in vitro data presented demonstrate that JTX-2011 alone induces a cytokine response from CD4 T cells, only if the T cells have pre-existing ICOS hi characteristics.
CTLA-4 inhibition has been shown to induce a population of ICOS hi cells in the bloodstream, while PD-1 inhibitors do not, and these observations further support the biological rationale for the ongoing clinical development of JTX-2011 in combination with ipilimumab.
In a poster titled "Inducible T cell Co-stimulator (ICOS) is upregulated on lymphocytes following radiation of tumors and ICOS agonism in combination with radiation results in enhanced tumor control," Jounce collaborators at the Earle A. Chile’s Research Institute, Providence Portland Medical Center, highlight the benefit of upregulation of ICOS in circulating and intra-tumoral T cells by radiation and its role in effective combination treatment with an ICOS agonist antibody to mediate tumor reduction. The data presented demonstrate:

The combination of radiation therapy and treatment with an ICOS agonist antibody led to increased anti-tumor response in an immunogenic mouse tumor model.
In a less immunogenic tumor model, response required the combination of ICOS agonist and PD-1 antagonist with radiation, suggesting again that ICOS agonism in combination with modalities that upregulate ICOS, such as with radiation, may represent an attractive regimen for combination immunotherapy of anti-PD-1 resistant tumors.
Both posters are available on the Investors and Media section of the Jounce Therapeutics website under "Presentations & Publications" at www.jouncetx.com.

About JTX-2011
Jounce’s lead product candidate, JTX-2011, is a monoclonal antibody that binds to and activates ICOS, a protein on the surface of certain T cells. Preclinical data support that JTX-2011 may have a dual mechanism of action that stimulates anti-tumor T effector cells, and also reduces the immunosuppressive T regulatory cells in the tumor microenvironment. The company is developing JTX-2011 to treat solid tumors as a single agent and in combination with other therapies.

Omeros Announces Pricing of $210 Million Offering of Convertible Senior Notes Due 2023

On November 9, 2018 Omeros Corporation (Nasdaq: OMER) ("Omeros") reported the pricing of an offering of $210 million aggregate principal amount of its 6.25% Convertible Senior Notes due 2023 (the "Notes") in a private offering (the "Offering") to qualified institutional buyers pursuant to Rule 144A under the Securities Act of 1933 (the "Securities Act") (Press release, Omeros, NOV 9, 2018, View Source;p=irol-newsArticle_Print&ID=2376484 [SID1234531091]). Omeros has granted the initial purchasers of the Notes an option to purchase up to an additional $40 million aggregate principal amount of the Notes on the same terms and conditions referenced above.

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The Notes will be senior unsecured obligations of Omeros and interest will be payable semi-annually in arrears at a rate of 6.25% per annum. The Notes will mature on November 15, 2023, unless converted, repurchased or redeemed in accordance with their terms prior to such date. The Notes will be convertible, upon the satisfaction of certain conditions or during specified periods, into cash, shares of Omeros’ common stock or a combination thereof as Omeros elects at its sole discretion. Omeros will have the right to redeem the Notes on or after November 15, 2019, subject to certain conditions.

The initial conversion rate of the Notes is 52.0183 shares of Omeros’ common stock per $1,000 principal amount of the Notes, which is equivalent to an initial conversion price of approximately $19.22 per share of Omeros’ common stock, and is subject to adjustment in certain circumstances. This initial conversion price represents a premium of approximately 20% over the last reported sale price on November 8, 2018 of Omeros’ common stock of $16.02 per share. Omeros has entered into the capped call transaction described below in order to avoid dilution to Omeros’ shareholders from conversions of the Notes if Omeros’ common stock price does not exceed $28.8360, which represents a premium of 80% over the last reported sale price of Omeros’ common stock.

The aggregate gross proceeds to Omeros from the offering of the Notes will be $210 million, exclusive of any proceeds attributable to the initial purchasers’ possible exercise of their option to purchase additional Notes. Omeros intends to use a portion of the net proceeds of the offering to repay in full the amounts outstanding under Omeros’ secured Term Loan Agreement with CRG Servicing LLC (the "Term Loan Agreement"), which has an annual interest rate of 12.25% and matures on September 30, 2022. Amounts repaid will include all accrued but unpaid interest and prepayment fees under the Term Loan Agreement.

Cantor Fitzgerald & Co. and UBS Investment Bank are acting as joint bookrunners for the offering. Cantor Fitzgerald & Co. is also acting as the sole structuring advisor for the offering.

In connection with the pricing of the Notes, Omeros entered into a capped call transaction with Royal Bank of Canada, or RBC. The capped call transaction is intended to minimize the potential dilution of Omeros’ common stock and/or offset potential cash payments in excess of the principal amount of the converted Notes upon conversion of the Notes, as Omeros elects at its sole discretion, in the event that the market price per share of Omeros’ common stock, as measured under the terms of the capped call transaction, is greater than the strike price of the capped call transaction, which initially corresponds to the conversion price of the Notes and is subject to anti-dilution adjustments substantially similar to those applicable to the conversion rate of the Notes. If, however, the market price per share of Omeros’ common stock, as measured under the terms of the capped call transaction, exceeds the cap price of the capped call transaction, there would nevertheless, upon conversion, be dilution or a cash expenditure, as elected by Omeros in its sole discretion, to the extent that such market price exceeds the cap price of the capped call transaction. The cap price under the capped call transaction will initially be $28.8360 per share, which represents a premium of 80% over the last reported sale price of Omeros’ common stock on November 8, 2018, and is subject to certain adjustments under the terms of the capped call transaction. If the initial purchasers exercise their option to purchase additional Notes, Omeros expects to enter into an additional capped call transaction.

Omeros has been advised that, in connection with establishing its initial hedge of the capped call transaction, RBC and/or its affiliates expect to enter into various derivative transactions with respect to Omeros’ common stock concurrently with or shortly after the pricing of the Notes. This activity could increase (or reduce the size of any decrease in) the market price of Omeros’ common stock or the Notes at that time. In addition, Omeros has been advised that RBC and/or its affiliates may modify their hedge positions by entering into or unwinding various derivatives with respect to Omeros’ common stock and/or purchasing or selling Omeros’ common stock in secondary market transactions following the pricing of the Notes and prior to the maturity of the Notes (and are likely to do so during any observation period related to a conversion of Notes). This activity could also cause or avoid an increase or a decrease in the market price of Omeros’ common stock or the Notes.

In addition to repaying the Term Loan Agreement and entering into the capped call transaction, Omeros intends to use the remainder of the net proceeds of the offering for general corporate purposes, including funding research and development for Omeros’ OMS721 programs and clinical trials, pre-clinical studies, manufacturing and other costs associated with advancing Omeros’ product candidates toward Marketing Authorization Application, Biologics License Application and New Drug Application submissions. If the initial purchasers exercise their option to purchase additional notes, then Omeros intends to use the additional net proceeds to fund the cost of entering into any additional capped call transactions and for general corporate purposes as described above. The offering is expected to close on November 15, 2018, subject to customary closing conditions.

This press release does not constitute an offer to sell or the solicitation of an offer to buy any securities of Omeros. Any offers of the Notes will be made only by means of a private offering memorandum. The offer and sale of the Notes and any shares of Omeros common stock issuable upon conversion of the Notes have not been, and will not be, registered under the Securities Act or the securities laws of any other jurisdiction, and the Notes and such shares may not be offered or sold in the United States absent registration or an applicable exemption from the Securities Act and applicable state laws.

Obsidian Presents Preclinical Data Demonstrating Precise Regulation of Cytokines and CAR in T cells with Destabilizing Domain Technology using FDA-Approved Drugs

On November 9, 2018 Obsidian Therapeutics, Inc., a biotechnology company developing cell therapies with pharmacologic operating systems, reported the presentation of preclinical data demonstrating fine-tuned regulation of cytokine production and CAR-T function using Destabilizing Domains (DDs) paired with FDA-approved small molecule drugs (Press release, Obsidian Therapeutics, NOV 9, 2018, View Source [SID1234531107]). Obsidian will reveal a suite of novel human DDs and showcase their application in CAR-T therapy at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s (SITC) (Free SITC Whitepaper) 33rd Annual Meeting in Washington, DC, November 7-11, 2018.

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DDs are small, fully-human protein domains that confer conditional stability to a fused payload protein. These regulated cassettes can be readily added to a cell or gene therapy product. CAR-T cells are engineered to find and destroy tumor cells and can be armed with powerful cytokines, such as IL12 and IL15, to further enhance anti-tumor immunity. However, these potent immune modulators require precise control to optimize their therapeutic benefit.

"Pharmacologic regulation of CAR-T therapies is a critical next step in the advancement of adoptive immunotherapy for cancer," said Steve Shamah, Ph.D., Senior Vice President and Head of Research for Obsidian, who will present one of the posters at SITC (Free SITC Whitepaper)’s 33rd Annual Meeting. "By designing pharmacologic operating systems that use FDA-approved small molecules for regulation, we believe we have opened a new set of opportunities for next-generation cell therapies."

Highlights of the two preclinical presentations describing Obsidian’s enhanced CAR-T therapies include:

Abstract Number P271: Titratable and reversible regulation of IL12 or IL15 with FDA-approved drugs for enhanced CAR-T therapy
Presenter: Steve Shamah, Ph.D.
Date and Time: Friday, November 9, from 12:45 – 2:15 pm and 6:30 – 8 pm

Our discovery process yields a wide array of fully human DD variants with performance characteristics that can be matched to specific applications.
We have achieved titratable, fine-tuned regulation of IL12 and IL15 in human T cells in vitro and in vivo with clinically translatable DDs and FDA-approved drugs.
Abstract Number P238: Regulation of in vivo anti-tumor activity of adoptively transferred CAR-T cells using FDA-approved small molecule drugs
Presenter: Jennifer Gori, Ph.D., Associate Director, Head of In Vivo Pharmacology, Obsidian
Date and Time: Saturday, November 10, from 12:20 – 1:50 pm and 7:00 – 8:30 pm

DDs provide small molecule regulation of CAR expression and activity in T cells.
We have demonstrated on-demand anti-tumor activity of a clinically translatable DD-CAR in T cells with drug dosing in vivo.
These studies show Obsidian’s ability to achieve precise kinetic and dose-responsive control over transgene-derived protein expression, fueling the development of CAR-T cell therapies that are potentially safer and more efficacious.

About Destabilizing Domains

Obsidian uses Destabilizing Domains (DDs) to enable pharmacologic regulation of protein activity for next-generation cell and gene therapies. Obsidian’s DDs are small, fully-human protein domains that confer conditional stability to a fused payload protein. In the absence of a specific small-molecule ligand, the fusion protein is rapidly degraded, whereas in the presence of the ligand the fusion protein becomes stable and functional. Obsidian uses this approach to equip engineered cells with controllable functions that can be precisely tuned by the administration of non-immunosuppressive, small-molecule medicines that are readily available and dispensed by the treating physician.