Skip to main content

23andMe Announces Three Presentations from Clinical-Stage Immuno-Oncology Programs at the American Association for Cancer Research (AACR) Annual Meeting 2024

23andMe to give an oral presentation on the genetic signature of ULBP6, the target of 23ME-01473, along with poster presentations of the biology of ULBP6 and mechanism of 23ME-01473, and new non-clinical insights for 23ME-00610, targeting the CD200R1 pathway

SOUTH SAN FRANCISCO, Calif., March 05, 2024 (GLOBE NEWSWIRE) — 23andMe Holding Co. (Nasdaq: ME) (“23andMe”), a leading human genetics and biopharmaceutical company, today announced an oral presentation and two poster presentations on two of the Company’s immuno-oncology programs that will be presented at the American Association for Cancer Research (AACR) Annual Meeting 2024, taking place in San Diego, CA, April 5-10, 2024.

The oral presentation will detail the use of the 23andMe genetic and health survey database to discover ULBP6, the highest affinity ligand of the NK and T-cell activation receptor, NKG2D. ULBP6 is the primary target for 23ME-01473 (‘1473), a dual mechanism monoclonal antibody. The Company will also present a poster on the biology of ULBP6, and how ‘1473 reinvigorates anti-tumor NK cell function through NKG2D and FcγRIIIa activation.

These presentations will be the first scientific communications the Company has prepared on ‘1473 since announcing its pursuit of this novel, genetically-validated target. The FDA recently cleared the IND application for ‘1473, which targets ULBP6. Cancers escape immune cell recognition by shedding ULBP ligands from their cell surface, which act as immunosuppressive molecular decoys. Blocking the binding of soluble ULBP6 to NKG2D with ‘1473 may restore immune cell recognition and killing of cancers. Further, ‘1473 is Fc-effector enhanced, which provides an additional mechanism for NK cells to induce cell death of ULBP6-expressing cancer cells.

23andMe will also present a non-clinical poster on 23ME-00610, an inhibitor of the CD200R1 receptor, which will include new insights into targeting the CD200R1 pathway in T and NK cells using 23ME-00610 as a single agent or in combination with other anti-tumor therapies. 23ME-00610 is currently in Phase 2a of a Phase 1/2a clinical study.

The presentations will be available on the 23andMe Investor Relations and Therapeutics websites on April 5, 2024.

Presentation details – 23ME-01473:

Oral presentation

  • Title: Discovery of ULBP6 as a novel immuno-oncology target using pleiotropic signals from 23andMeʼs genetic and health survey database
  • Session Type: Minisymposium
  • Session Category: Experimental and Molecular Therapeutics
  • Session Title: Drug Discovery 1: New Targets and Approaches
  • Session Date and Time: Monday, April 8, 2024, 2:30 – 4:30 PM PT
  • Published Abstract Number: 3903

Poster presentation

  • Title: 23ME-01473, a novel anti-ULBP6/2/5 monoclonal antibody, reinvigorates anti-tumor NK cell function through NKG2D and FcγRIIIa activation
  • Session Category: Clinical Research
  • Session Title: Antibodies 1
  • Session Date and Time: Monday, April 8, 2024, 9:00 AM – 12:30 PM PT
  • Location: Poster Section 38
  • Poster Board Number: 21
  • Published Abstract Number: 2375

Presentation Details: 23ME-00610:

Poster presentation

  • Title: New insights into targeting the CD200R1 pathway in T and NK cells using 23ME-00610 as a single agent or in combination
  • Session Category: Clinical Research
  • Session Title: Antibodies 1
  • Session Date and Time: Monday, April 8, 2024, 9:00 AM – 12:30 PM PT
  • Location: Poster Section 38
  • Poster Board Number: 5
  • Published Abstract Number: 2359

About 23ME-01473 (‘1473)
‘1473 targets ULBP6 to restore anti-tumor immunity through NK and T cells. ULBPs are stress-induced ligands found on the surface of cancer cells that bind to their receptor, NKG2D, on NK and T cells. Cancers escape immune cell recognition by shedding ULBP ligands from their cell surface, which act as immunosuppressive molecular decoys. Blocking the binding of soluble ULBP6 to NKG2D may restore immune cell recognition and killing of cancers. Further, ‘1473 is Fc-effector enhanced, which provides an additional mechanism for NK cells to induce cell death of ULBP6-expressing cancer cells. 23andMe plans to evaluate ‘1473 in participants with advanced solid tumors in a Phase 1 clinical study beginning in the first half of 2024. Clinical trials registry (clinicaltrials.gov): NCT06290388.

About 23ME-00610
23ME-00610 is a high-affinity, fully humanized monoclonal antibody that is designed to bind to CD200R1 and prevent the interaction of CD200R1 with CD200. The CD200–CD200R1 axis is an immunological checkpoint that plays a pivotal role in maintenance of immune tolerance. CD200R1 is an inhibitory receptor expressed on T cells and myeloid cells while CD200, the ligand for CD200R1, is highly expressed on certain tumors. In preclinical studies, binding of tumor-associated CD200 to CD200R1 leads to immune suppression and decreased immune cell killing of cancer cells. Preclinical data indicate that this mechanism has the potential to restore the ability for both T-cells and myeloid cells to kill cancer cells. Clinical trials registry (clinicaltrials.gov): NCT05199272.

About 23andMe
23andMe is a genetics-led consumer healthcare and biopharmaceutical company empowering a healthier future. For more information, please visit www.23andMe.com

Forward-Looking Statements
This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended, including, without limitation, statements regarding the future plans of 23andMe’s therapeutics business. All statements, other than statements of historical fact, included or incorporated in this press release, including statements regarding 23andMe’s strategy, the plans for and results of its clinical trials and objectives of management, are forward-looking statements. The words “believes,” “anticipates,” “estimates,” “plans,” “expects,” “intends,” “may,” “could,” “should,” “potential,” “likely,” “projects,” “predicts,” “continue,” “will,” “schedule,” and “would” or, in each case, their negative or other variations or comparable terminology, are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. These forward-looking statements are predictions based on 23andMe’s current expectations and projections about future events and various assumptions. 23andMe cannot guarantee that it will actually achieve the plans, intentions, or expectations disclosed in its forward-looking statements and you should not place undue reliance on 23andMe’s forward-looking statements. These forward-looking statements involve a number of risks, uncertainties (many of which are beyond the control of 23andMe), or other assumptions that may cause actual results or performance to differ materially from those expressed or implied by these forward-looking statements. The forward-looking statements contained herein are also subject generally to other risks and uncertainties that are described from time to time in the Company’s filings with the Securities and Exchange Commission, including under Item 1A, “Risk Factors” in the Company’s most recent Annual Report on Form 10-K, as filed with the Securities and Exchange Commission, and as revised and updated by our Quarterly Reports on Form 10-Q and Current Reports on Form 8-K. The statements made herein are made as of the date of this press release and, except as may be required by law, 23andMe undertakes no obligation to update them, whether as a result of new information, developments, or otherwise.

Contacts:
Investor Relations Contact: investors@23andMe.com
Media Contact: press@23andMe.com

Disclaimer & Cookie Notice

Welcome to GOLDEA services for Professionals

Before you continue, please confirm the following:

Professional advisers only

I am a professional adviser and would like to visit the GOLDEA CAPITAL for Professionals website.

Cookie Notice

We use cookies to improve your experience on our website

Information we collect about your use of Goldea Capital website

Goldea Capital website collects personal data about visitors to its website.

When someone visits our websites, we use a third party service, Google Analytics, to collect standard internet log information (such as IP address and type of browser they’re using) and details of visitor behavior patterns. We do this to allow us to keep track of the number of visitors to the various parts of the sites and understand how our website is used. We do not make any attempt to find out the identities or nature of those visiting our websites. We won’t share your information with any other organizations for marketing, market research or commercial purposes and we don’t pass on your details to other websites.

Use of cookies
Cookies are small text files that are placed on your computer or other device by websites that you visit. They are widely used to make websites work, or work more efficiently, as well as to provide information to the owners of the site.