Kolltan Pharmaceuticals Announces Presentations of Anti-KIT Antibody Preclinical Data at the 2016 American Association for Cancer Research (AACR) Annual Meeting

On April 20, 2016 Kolltan Pharmaceuticals, Inc., a privately held clinical-stage company focused on the discovery and development of novel antibody-based drugs targeting receptor tyrosine kinases (RTKs) for use in oncology and immunology, reported the presentation of preclinical data relating to its KTN0158 drug development program at the AACR (Free AACR Whitepaper) Annual Meeting, taking place in New Orleans, Louisiana, April 16-20, 2016 (Press release, Kolltan Pharmaceuticals, APR 20, 2016, View Source [SID:1234511162]). KTN0158 is a proprietary, clinical-stage, humanized anti-KIT IgG1 monoclonal antibody drug candidate that selectively and potently inhibits KIT and is being developed as a potential therapy for cancer and mast cell-related diseases.

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"The compelling preclinical data that were presented at AACR (Free AACR Whitepaper) support our plans to evaluate KTN0158 in combination with T-cell checkpoint inhibitors in the clinic near-term. This expands our current clinical focus beyond gastrointestinal stromal tumors (GIST) and further broadens the opportunity to investigate the treatment of cancer patients through targeting KIT, with potential to affect immunosuppressive mast cells and myeloid cells. Developing innovative biologics with a focus on RTKs expressed on innate immune cells is an exciting new area for Kolltan with KTN0158 in clinical development," stated Gerald McMahon, Ph.D., President and Chief Executive Officer of Kolltan.

Rich Gedrich, Ph.D., Senior Director of Translational Medicine of Kolltan, added, "KTN0158 represents a novel approach to inhibit KIT on tumor cells by blocking the dimerization of the receptor through an allosteric mechanism. Previous preclinical data have shown significant anti-tumor activity in KIT-driven tumors such as GIST, targeted in our Phase 1 trial of KTN0158, and now the current findings in combination with anti-PD-1 and anti-CTLA4 antibodies support a second distinct approach to develop KTN0158 as an anti-cancer therapy."

Following are the key data and results from the two presentations at AACR (Free AACR Whitepaper) relating to KTN0158:
On Sunday, April 17, KTN0158 was highlighted as a novel experimental treatment approach for GIST in an oral presentation titled "Experimental Treatment Options for Gastrointestinal Stromal Tumors with Primary or Secondary Resistance to Tyrosine Kinase Inhibitors". The presentation reviewed previously disclosed preclinical data including:

An overview of KTN0158’s unique mechanism of action which inhibits KIT activation by blocking receptor dimerization; and
The preclinical activity of KTN0158 in GIST models with activating KIT mutations and also activity in dogs with spontaneous mast cell tumors driven by KIT activation.

On Tuesday, April 19, "Inhibition of KIT In Vivo Modifies Immune Cell Populations to Improve the Efficacy of Checkpoint Inhibitors in Syngeneic Mouse Tumor Models" (Abstract Number 4020), was presented in a poster session.

The poster presentation reported the following data and results:

Enhanced anti-tumor activity with the combination of a surrogate mouse anti-KIT monoclonal antibody with either anti-PD-1 or anti-CTLA4 monoclonal antibodies in several syngeneic mouse tumor models; and

Mechanistic studies showed a significant decrease in monocytic myeloid-derived suppressor cells (mMDSCs) in the tumor and in the spleen of the anti-KIT antibody treated groups. High levels of circulating mMDSCs have been associated with reduced survival in melanoma patients treated with ipilimumab or nivolumab.

The poster is available on the Kolltan website.

About KTN0158

KTN0158 is a proprietary, humanized monoclonal antibody designed using structure-based approaches to block the activation of KIT, an RTK that is expressed on many cancers and mast cells. There are currently no KIT-targeting antibodies on the market for any disease indication. In oncology, KIT is expressed in tumors such as GIST, melanoma, acute myeloid leukemia (AML), small cell lung cancer (SCLC), and others. Additionally, KIT is expressed in immune suppressive cells in the tumor microenvironment and thus may provide a novel combination treatment for immuno-oncology. Kolltan has initiated a Phase 1 study for the treatment of GIST and other KIT-expressing tumors (NCT02642016) and plans to move into combination studies with other targeted therapies and T cell checkpoint inhibitors.

Joint modelling of longitudinal and multi-state processes: application to clinical progressions in prostate cancer.

Joint modelling of longitudinal and survival data is increasingly used in clinical trials on cancer. In prostate cancer for example, these models permit to account for the link between longitudinal measures of prostate-specific antigen (PSA) and time of clinical recurrence when studying the risk of relapse. In practice, multiple types of relapse may occur successively. Distinguishing these transitions between health states would allow to evaluate, for example, how PSA trajectory and classical covariates impact the risk of dying after a distant recurrence post-radiotherapy, or to predict the risk of one specific type of clinical recurrence post-radiotherapy, from the PSA history. In this context, we present a joint model for a longitudinal process and a multi-state process, which is divided into two sub-models: a linear mixed sub-model for longitudinal data and a multi-state sub-model with proportional hazards for transition times, both linked by a function of shared random effects. Parameters of this joint multi-state model are estimated within the maximum likelihood framework using an EM algorithm coupled with a quasi-Newton algorithm in case of slow convergence. It is implemented under R, by combining and extending mstate and JM packages. The estimation program is validated by simulations and applied on pooled data from two cohorts of men with localized prostate cancer. Thanks to the classical covariates available at baseline and the repeated PSA measurements, we are able to assess the biomarker’s trajectory, define the risks of transitions between health states and quantify the impact of the PSA dynamics on each transition intensity. Copyright © 2016 John Wiley & Sons, Ltd.
Copyright © 2016 John Wiley & Sons, Ltd.

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Adjuvant ovarian function suppression and cognitive function in women with breast cancer.

To examine the effect on cognitive function of adjuvant ovarian function suppression (OFS) for breast cancer.
The Suppression of Ovarian Function (SOFT) trial randomised premenopausal women with hormone receptor-positive breast cancer to 5 years adjuvant endocrine therapy with tamoxifen+OFS, exemestane+OFS or tamoxifen alone. The Co-SOFT substudy assessed objective cognitive function and patient reported outcomes at randomisation (T0), and 1 year later (T1); the primary endpoint was change in global cognitive function, measured by the composite objective cognitive function score. Data were compared for the pooled tamoxifen+OFS and exemestane+OFS groups vs the tamoxifen alone group using the Wilcoxon rank-sum test.
Of 86 participants, 74 underwent both T0 and T1 cognitive testing; 54 randomised to OFS+ either tamoxifen (28) or exemestane (26) and 20 randomised to tamoxifen alone. There was no significant difference in the changes in the composite cognitive function scores between the OFS+ tamoxifen or exemestane groups and the tamoxifen group (mean±s.d., -0.21±0.92 vs -0.04±0.49, respectively, P=0.71, effect size=-0.20), regardless of prior chemotherapy status, and adjusting for baseline characteristics.
The Co-SOFT study, although limited by small samples size, provides no evidence that adding OFS to adjuvant oral endocrine therapy substantially affects global cognitive function.British Journal of Cancer advance online publication 19 April 2016; doi:10.1038/bjc.2016.71 www.bjcancer.com.

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CCN4/WISP1 (WNT1 inducible signaling pathway protein 1): a focus on its role in cancer.

The matricellular protein WISP1 is a member of the CCN protein family. It is induced by WNT1 and is a downstream target of β-catenin. WISP1 is expressed during embryonic development, wound healing and tissue repair. Aberrant WISP1 expression is associated with various pathologies including osteoarthritis, fibrosis and cancer. Its role in tumor progression and clinical outcome makes WISP1 an emerging candidate for the detection and treatment of tumors.
Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.

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Phase I Study of the Prolactin Receptor Antagonist LFA102 in Metastatic Breast and Castration-Resistant Prostate Cancer.

Despite evidence for a role for prolactin signaling in breast and prostate tumorigenesis, a prolactin receptor-binding monoclonal antibody has not produced clinical efficacy.Increased serum prolactin levels may be a biomarker for prolactin receptor inhibition.Results from the pharmacokinetic and pharmacodynamics (PD) studies suggest that inappropriately long dosing intervals and insufficient exposure to LFA102 may have resulted in lack of antitumor efficacy.Based on preclinical data, combination therapy of LFA102 with those novel agents targeting hormonal pathways in metastatic castration-resistant prostate cancer and metastatic breast cancer is promising.Given the PD evidence of prolactin receptor blockade by LFA102, this drug has the potential to be used in conditions such as hyperprolactinemia that are associated with high prolactin levels.
Prolactin receptor (PRLR) signaling is implicated in breast and prostate cancer. LFA102, a humanized monoclonal antibody (mAb) that binds to and inhibits the PRLR, has exhibited promising preclinical antitumor activity.
Patients with PRLR-positive metastatic breast cancer (MBC) or metastatic castration-resistant prostate cancer (mCRPC) received doses of LFA102 at 3-60 mg/kg intravenously once every 4 weeks. Objectives were to determine the maximum tolerated dose (MTD) and/or recommended dose for expansion (RDE) to investigate the safety/tolerability of LFA102 and to assess pharmacokinetics (PK), pharmacodynamics (PD), and antitumor activity.
A total of 73 patients were enrolled at 5 dose levels. The MTD was not reached because of lack of dose-limiting toxicities. The RDE was established at 60 mg/kg based on PK and PD analysis and safety data. The most common all-cause adverse events (AEs) were fatigue (44%) and nausea (33%) regardless of relationship. Grade 3/4 AEs reported to be related to LFA102 occurred in 4% of patients. LFA102 exposure increased approximately dose proportionally across the doses tested. Serum prolactin levels increased in response to LFA102 administration, suggesting its potential as a biomarker for PRLR inhibition. No antitumor activity was detected.
Treatment with LFA102 was safe and well tolerated, but did not show antitumor activity as monotherapy at the doses tested.
©AlphaMed Press; the data published online to support this summary is the property of the authors.

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