Tyra Biosciences to Present Preclinical Data on TYRA-200, an FGFR1/2/3 Inhibitor, at 34th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics

Rhea-AI Summary

Tyra Biosciences (Nasdaq: TYRA) will present preclinical data on its FGFR1/2/3 inhibitor, TYRA-200, at the 34th EORTC-NCI-AACR Symposium in Barcelona, Spain, from October 26-28, 2022. The presentation is scheduled for October 26 and focuses on TYRA-200's effectiveness against FGFR2 fusions, molecular brake mutations, and gatekeeper resistance, with the aim of enhancing outcomes for cancer patients. This event is pivotal as the company seeks to advance its pipeline targeting critical genetic alterations affecting cancer treatment.

Positive

• Presentation of promising preclinical data on TYRA-200 at a major cancer symposium.
• TYRA-200 shows potency against FGFR2 fusions and resistance mutations, indicating potential for improved cancer therapies.

Negative

• None.

CARLSBAD, Calif., Oct. 13, 2022 /PRNewswire/ -- Tyra Biosciences, Inc. (Nasdaq: TYRA), a precision oncology company focused on developing purpose-built therapies to overcome tumor resistance and improve outcomes for patients with cancer, today announced that the Company will present preclinical data on TYRA-200 during a poster session at the 34^th EORTC-NCI-AACR Symposium on Molecular Targets and Cancer Therapeutics, taking place October 26-28, 2022, in Barcelona, Spain.

Details of the poster presentation are as follows:

Title:  TYRA-200: Potent Against FGFR2 Fusions, Molecular Brake Mutations and Gatekeeper Resistance
Date/Time/Location: Wednesday, October 26, 2022, 12-20:00 CET, Exhibition Hall
Session/Session Code: Molecular Targeted Agents 1, PP20
Poster #: 47

Regular abstracts are available on the EORTC-NCI-AACR website.  The poster on TYRA-200 will be made available on the TYRA website under the "For Investors" section on October 26, 2022.

About Tyra Biosciences

Tyra Biosciences, Inc. is a precision oncology company focused on developing purpose-built therapies to overcome tumor resistance and improve outcomes for patients with cancer. TYRA's proprietary in-house discovery platform, SNÅP, enables the rapid and precise refinement of structural design through iterative molecular SNÅPshots that help predict genetic alterations most likely to cause acquired resistance to existing therapies.  Leveraging SNÅP, TYRA is developing a pipeline of selective inhibitors of Fibroblast Growth Factor Receptors (FGFR), which are altered in approximately 7% of all cancers.  TYRA-300 is an FGFR3 selective inhibitor for oncology.  TYRA-200 is an FGFR1/2/3 inhibitor with potency against FGFR2 fusions, molecular brake mutations and gatekeeper resistance that TYRA is developing initially in intrahepatic cholangiocarcinoma. TYRA is also targeting achondroplasia and other FGFR3-related skeletal dysplasias and FGFR4 and REarranged during Transfection kinase (RET) related cancers. TYRA is based in Carlsbad, CA.  For more information about our science, pipeline and people, please visit www.tyra.bio and engage with us on LinkedIn.

Contact:

Amy Conrad
aconrad@tyra.bio

 

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SOURCE Tyra Biosciences, Inc.

FAQ

What is the purpose of the TYRA-200 presentation at the EORTC-NCI-AACR Symposium?

The presentation aims to showcase preclinical data on TYRA-200's effectiveness against FGFR2 fusions and mutations related to tumor resistance.

When will Tyra Biosciences present data on TYRA-200?

Tyra Biosciences will present data on TYRA-200 on October 26, 2022, during the EORTC-NCI-AACR Symposium.

What are the key features of TYRA-200?

TYRA-200 is an FGFR1/2/3 inhibitor known for its potency against FGFR2 fusions and molecular resistance mutations.

Where can I find the poster presentation on TYRA-200?

The poster on TYRA-200 will be available on the Tyra Biosciences website under the 'For Investors' section on October 26, 2022.

What are the implications of the preclinical data on TYRA-200?

The preclinical data indicates potential advancements in therapy effectiveness, particularly for cancers driven by FGFR alterations.