Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

ePoster Display

1006P - ACE1702, a first-in-class, off-the-shelf, selected natural killer cell [oNK] product using antibody cell conjugation technology [ACC], with pre-clinical and early clinical activity in HER2 < 3+ tumors

Date

16 Sep 2021

Session

ePoster Display

Topics

Clinical Research;  Targeted Therapy;  Immunotherapy

Tumour Site

Presenters

Sarina Piha-Paul

Citation

Annals of Oncology (2021) 32 (suppl_5): S829-S866. 10.1016/annonc/annonc705

Authors

S.A. Piha-Paul1, D. Mahalingam2, M.F. Mulcahy2, A. Kalyan2, H. Li3, E. Wu3, M. Kurman3, S. Lee3, Y. Lin3, S. Tang3, C. Hsiao3, J. Pan3, S. Chien3

Author affiliations

  • 1 Department Of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, 77030 - Houston/US
  • 2 Robert H. Lurie Comprehensive Cancer Center, Northwestern Memorial Hospital, 60611 - Chicago/US
  • 3 R&d, Acepodia Inc, 94402 - San Mateo/US

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 1006P

Background

ACE1702 is manufactured with a proprietary low-cost method using oNK immortalized cell source with stable high expression of multiple NK activation receptors, including CD16, conjugated to anti-HER2 IgG via ACC, and low levels of inhibitory receptors. Preclinical in vitro & in vivo studies and initial data from Ph1 study (NCT04319757) of patients [pts] with advanced HER2 tumors will be presented.

Methods

ACE1702 activity was evaluated by in vitro cytotoxicity assay and in vivo xenograft model to enable a multicenter Ph1 study to evaluate safety, PK/PD, and antitumor response and define a recommended Ph2 dose. Up to 36 pts with advanced HER2 IHC ≥ 2+ tumors are to be enrolled to receive low dose lymphodepletion [LD] followed by an assigned level of escalating ACE1702 doses 0.3-15 billion [B] cells/cycle. [Total cycle dose delivered in 3 infusions].

Results

In vitro, ACE1702 lysed 3 cell lines [1+ - 3+ HER2] using low effector:target ratios. In NSG xenografts, ACE1702 suppressed HER2 tumor growth by Day 4 and through the 29-day study using 2 infusions/week x 3 weeks. By MAR2021, 7pts received 0.3-3B cells/cycle and were evaluable for toxicity and response. Common AEs were lymphopenia (n=6), leukopenia (n=4), neutropenia (n=4) [all due to LD] and fatigue (n=4) [1 Gr1 related to drug] and all improved by 30 days post-drug. No dose limiting toxicity [DLT], cytokine release syndrome [CRS], neurotoxicity or graft vs. host disease [GvHD] was observed. Only 1 SAE [pulmonary embolism], unrelated to drug, was reported. At 3B cells/cycle, peak blood concentrations occurred at 4hrs post initial infusion, and detectable up to 48hrs. At 3B cells/cycle, 1 pt with HER2 2+ refractory salivary gland tumor achieved a partial response by RECIST with increased serum IFNγ and IL10, but not IL6.

Conclusions

In pre-clinical studies, ACE1702 exhibited cancer-specific cytotoxicity and superior potency against low HER2 tumors. Preliminary data in pts showed no CRS, GvHD, or DLTs through doses of 3B cells/cycle and antitumor activity in a HER2 < 3+ tumor. Dose escalation continues up to 15B cells/cycle with updated clinical data to be provided.

Clinical trial identification

NCT04319757.

Editorial acknowledgement

Legal entity responsible for the study

Acepodia Inc.

Funding

Acepodia Inc.

Disclosure

S.A. Piha-Paul: Non-Financial Interests, Institutional, Research Grant: AbbVie, Inc.; Non-Financial Interests, Institutional, Research Grant: ABM Therapeutics, Inc.; Non-Financial Interests, Institutional, Research Grant: Acepodia, Inc; Non-Financial Interests, Institutional, Research Grant: Alkermes; Non-Financial Interests, Institutional, Research Grant: Aminex Therapeutics; Non-Financial Interests, Institutional, Research Grant: Amphivena Therapeutics, Inc.; Non-Financial Interests, Institutional, Research Grant: BioMarin Pharmaceutical, Inc; Non-Financial Interests, Institutional, Research Grant: Boehringer Ingelheim; Non-Financial Interests, Institutional, Research Grant: Bristol Myers Squib; Non-Financial Interests, Institutional, Research Grant: Cerulean Pharma, Inc.; Non-Financial Interests, Institutional, Research Grant: Chugai Pharmaceutical Co., Ltd; Non-Financial Interests, Institutional, Research Grant: Curis, Inc.; Non-Financial Interests, Institutional, Research Grant: Daiichi Sankyo; Non-Financial Interests, Institutional, Research Grant: Eli Lilly; Non-Financial Interests, Institutional, Research Grant: ENB Therapeutics; Non-Financial Interests, Institutional, Research Grant: Five Prime Therapeutics; Non-Financial Interests, Institutional, Research Grant: F-Star Therapeutics; Non-Financial Interests, Institutional, Research Grant: Gene Quantum; Non-Financial Interests, Institutional, Research Grant: Genmab A/S; Non-Financial Interests, Institutional, Research Grant: GlaxoSmithKline; Non-Financial Interests, Institutional, Research Grant: Helix BioPharma Corp.; Non-Financial Interests, Institutional, Research Grant: Incyte Corp.; Non-Financial Interests, Institutional, Research Grant: Jacobio Pharmaceuticals Co., Ltd.; Non-Financial Interests, Institutional, Research Grant: Medimmune, LLC.; Non-Financial Interests, Institutional, Research Grant: Medivation, Inc.; Non-Financial Interests, Institutional, Research Grant: Merck Sharp and Dohme Corp.; Non-Financial Interests, Institutional, Research Grant: Novartis Pharmaceuticals; Non-Financial Interests, Institutional, Research Grant: Pieris Pharmaceuticals, Inc.; Non-Financial Interests, Institutional, Research Grant: Pfizer; Non-Financial Interests, Institutional, Research Grant: Principia Biopharma, Inc.; Non-Financial Interests, Institutional, Research Grant: Puma Biotechnology, Inc.; Non-Financial Interests, Institutional, Research Grant: Rapt Therapeutics, Inc.; Non-Financial Interests, Institutional, Research Grant: Seattle Genetics; Non-Financial Interests, Institutional, Research Grant: Silverback Therapeutics; Non-Financial Interests, Institutional, Research Grant: Taiho Oncology; Non-Financial Interests, Institutional, Research Grant: Tesaro, Inc.; Non-Financial Interests, Institutional, Research Grant: TransThera Bio; Non-Financial Interests, Institutional, Research Grant: NCI/NIH; Non-Financial Interests, Institutional, Research Grant: P30CA016672 – Core Grant. D. Mahalingam: Non-Financial Interests, Personal, Speaker’s Bureau: Amgen Inc.; Non-Financial Interests, Personal, Speaker’s Bureau: Eisai Co., Ltd.; Non-Financial Interests, Personal, Speaker’s Bureau: Exelixis, Inc.; Non-Financial Interests, Personal, Speaker’s Bureau: Bristol Myers Squib; Non-Financial Interests, Institutional, Research Grant: Acepodia Biotech Inc. H. Li: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. E. Wu: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. M. Kurman: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. S. Lee: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. Y. Lin: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. S. Tang: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. C. Hsiao: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. J. Pan: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. S. Chien: Financial Interests, Personal, Full or part-time Employment: Acepodia Inc. All other authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.