– 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 submit ACH Investigational New Drug Application (IND) in 2H24-
CARLSBAD, CA, USA I July 2, 2024 I 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.
HCH 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.
“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.”
In 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<0.01); tibia by 3.75% compared to the vehicle (p<0.05); humerus by 3.22% compared to the vehicle (p<0.05); and ulna by 5.03% compared to the vehicle (p<0.01). TYRA-300 also increased the size of the foramen magnum by 5.88% (p<0.05) in mice. TYRA-300 demonstrated binding against the FGFR3 N540K altered protein and isoform selectivity for FGFR3 over other isoforms, as previously reported.
“The improvements in growth plate function observed in the hypochondroplasia mouse model provide strong proof-of-concept supporting further development of TYRA-300 for hypochondroplasia,” said Dr. Michael Bober, VP, Clinical Development and Medical Affairs of TYRA. “This adds to the evidence of TYRA-300 becoming a potential precision medicine for FGFR3 mediated skeletal dysplasia.”
Susana Noval Iruretagoyena, Director, Fundación ALPE, commented, “It’s an exciting time for research in skeletal dysplasia and movement into hypochondroplasia. Like with achondroplasia, it will be important for companies to study more outcomes beyond height for these families.”
The presentation from the 6th Annual Achondroplasia & Skeletal Dysplasia Research Conference can be accessed here.
About TYRA-300
TYRA-300 is the Company’s lead precision medicine program stemming from its in-house SNÅP platform. TYRA-300 is an investigational, oral, FGFR3-selective inhibitor currently in development for the treatment of cancer and skeletal dysplasias, including achondroplasia. In oncology, TYRA-300 is being evaluated in a multi-center, open label Phase 1/2 clinical study, SURF301 (Study in Untreated and Resistant FGFR3+ Advanced Solid Tumors), which was designed to determine the recommended Phase 2 dose (RP2D) of TYRA-300, as well as to evaluate preliminary antitumor activity. In skeletal dysplasias, TYRA-300 has demonstrated positive preclinical results in achondroplasia and hypochondroplasia, and the Company expects to submit an IND in the second half of 2024 for the initiation of a Phase 2 clinical study in pediatric achondroplasia. In July 2023 and January 2024, the FDA granted Orphan Drug Designation (ODD) and Rare Pediatric Designation (RPD) to TYRA-300, respectively, for the treatment of achondroplasia.
About Tyra Biosciences
Tyra Biosciences, Inc. (Nasdaq: TYRA) is a clinical-stage biotechnology company focused on developing next-generation precision medicines that target large opportunities in FGFR biology. The Company’s in-house precision medicine platform, SNÅP, enables rapid and precise drug design through iterative molecular SNÅPshots that help predict genetic alterations most likely to cause acquired resistance to existing therapies. TYRA’s initial focus is on applying its accelerated small molecule drug discovery engine to develop therapies in targeted oncology and genetically defined conditions. 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.
SOURCE: Tyra Biosciences
Post Views: 485
– 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 submit ACH Investigational New Drug Application (IND) in 2H24-
CARLSBAD, CA, USA I July 2, 2024 I 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.
HCH 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.
“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.”
In 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<0.01); tibia by 3.75% compared to the vehicle (p<0.05); humerus by 3.22% compared to the vehicle (p<0.05); and ulna by 5.03% compared to the vehicle (p<0.01). TYRA-300 also increased the size of the foramen magnum by 5.88% (p<0.05) in mice. TYRA-300 demonstrated binding against the FGFR3 N540K altered protein and isoform selectivity for FGFR3 over other isoforms, as previously reported.
“The improvements in growth plate function observed in the hypochondroplasia mouse model provide strong proof-of-concept supporting further development of TYRA-300 for hypochondroplasia,” said Dr. Michael Bober, VP, Clinical Development and Medical Affairs of TYRA. “This adds to the evidence of TYRA-300 becoming a potential precision medicine for FGFR3 mediated skeletal dysplasia.”
Susana Noval Iruretagoyena, Director, Fundación ALPE, commented, “It’s an exciting time for research in skeletal dysplasia and movement into hypochondroplasia. Like with achondroplasia, it will be important for companies to study more outcomes beyond height for these families.”
The presentation from the 6th Annual Achondroplasia & Skeletal Dysplasia Research Conference can be accessed here.
About TYRA-300
TYRA-300 is the Company’s lead precision medicine program stemming from its in-house SNÅP platform. TYRA-300 is an investigational, oral, FGFR3-selective inhibitor currently in development for the treatment of cancer and skeletal dysplasias, including achondroplasia. In oncology, TYRA-300 is being evaluated in a multi-center, open label Phase 1/2 clinical study, SURF301 (Study in Untreated and Resistant FGFR3+ Advanced Solid Tumors), which was designed to determine the recommended Phase 2 dose (RP2D) of TYRA-300, as well as to evaluate preliminary antitumor activity. In skeletal dysplasias, TYRA-300 has demonstrated positive preclinical results in achondroplasia and hypochondroplasia, and the Company expects to submit an IND in the second half of 2024 for the initiation of a Phase 2 clinical study in pediatric achondroplasia. In July 2023 and January 2024, the FDA granted Orphan Drug Designation (ODD) and Rare Pediatric Designation (RPD) to TYRA-300, respectively, for the treatment of achondroplasia.
About Tyra Biosciences
Tyra Biosciences, Inc. (Nasdaq: TYRA) is a clinical-stage biotechnology company focused on developing next-generation precision medicines that target large opportunities in FGFR biology. The Company’s in-house precision medicine platform, SNÅP, enables rapid and precise drug design through iterative molecular SNÅPshots that help predict genetic alterations most likely to cause acquired resistance to existing therapies. TYRA’s initial focus is on applying its accelerated small molecule drug discovery engine to develop therapies in targeted oncology and genetically defined conditions. 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.
SOURCE: Tyra Biosciences
Post Views: 485
