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Tyra Biosciences Announces Preclinical Proof-of-Concept Results with TYRA-300 in Hypochondroplasia (HCH)
- In a preclinical HCH model, TYRA-300 demonstrated increases in long bone length and binding against the HCH altered protein- -TYRA remains on track to
About this update from Tyra Biosciences, Inc.
[{"type":"text","content":"- In a preclinical HCH model, TYRA-300 demonstrated increases in long bone length and binding against the HCH altered protein- \n-TYRA remains on track to submit ACH Investigational New Drug Application (IND) in 2H24-\nCARLSBAD, Calif., July 2, 2024 /PRNewswire/ -- Tyra Biosciences, Inc. (Nasdaq: TYRA), a clinical-stage biotechnology company focused on developing next-generation precision medicines that target large opportunities in Fibroblast Growth Factor Receptor (FGFR) biology, today announced preclinical proof-of-concept results with TYRA-300, an investigational oral FGFR3 selective inhibitor, in hypochondroplasia (HCH). The results were presented at the 6th Annual Achondroplasia & Skeletal Dysplasia Research Conference (Pharmachon 2024), held June 28-30, 2024, in Baltimore, MD.\nHCH is a skeletal dysplasia closely related to achondroplasia (ACH), the most common form of dwarfism. HCH is most commonly caused by the N540K mutation (~70-80%) in the FGFR3 gene. There are currently no approved therapeutic options for HCH. The design of TYRA-300 may inhibit the alteration driving FGFR3-related skeletal dysplasias including ACH, HCH and others.\n\"The new preclinical data presented at Pharmachon 2024 are very encouraging and continue to support our belief that TYRA-300 has the potential to become a best-in-class agent with the potential to address unmet medical needs for people with skeletal dysplasias,\" said Todd Harris, CEO of TYRA. \"Developing TYRA-300 in HCH is a natural extension of our plans in ACH, and we look forward to submitting our IND in the second half of this year to support our planned Phase 2 study in pediatric achondroplasia.\"\nIn an Fgfr3Asn534Lys/+ preclinical model, TYRA-300 was evaluated in FGFR3 wild-type and mutant animals to evaluate its potential effect on long bone length and skull size compared to vehicle-treated mice. TYRA-300 was administered daily at 1.8 mg/kg/day for 21 days starting at Day 3. TYRA-300 increased the length of the appendicular skeleton in the FGFR3 mutated mice: femur by 3.70% compared to the vehicle (p","length":2518,"tagName":"div"}]