G1 Therapeutics focuses on developing innovative cancer therapies, particularly through its lead product, Trilaciclib. This drug is a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor designed to protect bone marrow during chemotherapy, thereby reducing the incidence of chemotherapy-induced myelosuppression. Clinical studies have demonstrated that Trilaciclib can enhance patient outcomes by improving survival rates and reducing the need for supportive care interventions in patients with extensive-stage small cell lung cancer (ES-SCLC) and metastatic triple-negative breast cancer (mTNBC). The drug's ability to modulate the immune response and improve the tumor microenvironment is also being investigated, highlighting its potential to enhance the efficacy of other anticancer therapies.

In addition to its primary focus on Trilaciclib, G1 Therapeutics is actively engaged in a robust pipeline of clinical research, with numerous publications detailing the safety and efficacy of Trilaciclib in various cancer settings. The company has presented findings at major oncology conferences, showcasing the drug's benefits in real-world scenarios and its role in improving treatment patterns for patients undergoing chemotherapy. G1 Therapeutics is committed to advancing the understanding of myelosuppression and its management, aiming to deliver next-generation therapies that significantly improve the lives of cancer patients.

United States

G1 Therapeutics, Inc., is a clinical-stage biopharmaceutical company focused on the discovery, development and delivery of innovative therapies that improve the lives of those affected by cancer.

Cancer

G1 Therapeutics

Small cell lung cancer

Solid tumor/s

Trilaciclib is a small molecule, competitive inhibitor of cyclin dependent kinases 4 and 6 (CDK4/6), with potential antineoplastic and chemoprotective activities. Upon intravenous administration, trilaciclib binds to and inhibits the activity of CDK4/6, thereby blocking the phosphorylation of the retinoblastoma protein (Rb) in early G1. This prevents G1/S phase transition, causes cell cycle arrest in the G1 phase, induces apoptosis, and inhibits the proliferation of CDK4/6-overexpressing tumor cells. In patients with CDK4/6-independent tumor cells, G1T28 may protect against multi-lineage chemotherapy-induced myelosuppression (CIM) by transiently and reversibly inducing G1 cell cycle arrest in hematopoietic stem and progenitor cells (HSPCs) and preventing transition to the S phase. This protects all hematopoietic lineages, including red blood cells, platelets, neutrophils and lymphocytes, from the DNA-damaging effects of certain chemotherapeutics and preserves the function of the bone marrow and the immune system. CDKs are <a href="https://pubchem.ncbi.nlm.nih.gov/compound/serine" rel="follow">serine</a>/<a href="https://pubchem.ncbi.nlm.nih.gov/compound/threonine" rel="follow">threonine</a> kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types. HSPCs are dependent upon CDK4/6 for proliferation.
<a href="https://pubchem.ncbi.nlm.nih.gov/compound/Trilaciclib#:~:text=Upon%20intravenous%20administration%2C%20trilaciclib%20binds,(Rb)%20in%20early%20G1.">source</a> - National Library of Medicine (National Institute of Health)

COSELA™ Trilaciclib (G1T28) (CDK4/6 inhibitor)

Breast cancer

Triple-negative breast cancer

Trilaciclib is a small molecule, competitive inhibitor of cyclin dependent kinases 4 and 6 (CDK4/6), with potential antineoplastic and chemoprotective activities. Upon intravenous administration, trilaciclib binds to and inhibits the activity of CDK4/6, thereby blocking the phosphorylation of the retinoblastoma protein (Rb) in early G1. This prevents G1/S phase transition, causes cell cycle arrest in the G1 phase, induces apoptosis, and inhibits the proliferation of CDK4/6-overexpressing tumor cells. In patients with CDK4/6-independent tumor cells, G1T28 may protect against multi-lineage chemotherapy-induced myelosuppression (CIM) by transiently and reversibly inducing G1 cell cycle arrest in hematopoietic stem and progenitor cells (HSPCs) and preventing transition to the S phase. This protects all hematopoietic lineages, including red blood cells, platelets, neutrophils and lymphocytes, from the DNA-damaging effects of certain chemotherapeutics and preserves the function of the bone marrow and the immune system. CDKs are <a href="https://pubchem.ncbi.nlm.nih.gov/compound/serine" rel="follow">serine</a>/<a href="https://pubchem.ncbi.nlm.nih.gov/compound/threonine" rel="follow">threonine</a> kinases involved in the regulation of the cell cycle and may be overexpressed in certain cancer cell types. HSPCs are dependent upon CDK4/6 for proliferation. (<a href="https://www.ncbi.nlm.nih.gov/">Source - National Library of Medicine National Center for Biotechnology Information)</a>

Trilaciclib (Cosela) (CDK4/6 inhibitor) 

Metastatic breast cancer

Trilaciclib (Cosela) + Trodelvy® (sacituzumab govitecan-hziy) (ADC)

Bladder cancer

Trilaciclib (Cosela) (CDK4/6 inhibitor) + avelumab

Trilaciclib (Cosela) (CDK4/6 inhibitor)

Rintodestrant&nbsp;is a potential best-in-class oral selective estrogen receptor degrader (SERD) in development for the treatment of estrogen receptor-positive (ER+) breast cancer.&nbsp;Preclinical data have shown rintodestrant&nbsp;to be more potent than fulvestrant, currently the only FDA-approved SERD. Unlike fulvestrant, which is administered as an intramuscular injection, rintodestrant&nbsp;has the potential to significantly improve the patient experience with oral dosing.&nbsp;In 2018, we initiated a Phase 1/2a trial of rintodestrant&nbsp;in estrogen receptor-positive, HER2-negative (ER+, HER2-) breast cancer (<a href="https://clinicaltrials.gov/ct2/show/NCT03455270?term=g1t48&amp;rank=1" target="_blank">NCT03455270</a>). We <a href="http://investor.g1therapeutics.com/news-releases/news-release-details/g1-therapeutics-presents-first-clinical-data-oral-serd-g1t48" target="_blank">reported the first clinical data</a> from this trial at the European Society for Medical Oncology (ESMO) 2019 Congress. In the second quarter of 2020, we initiated an additional arm of our ongoing Phase 1/2a trial to evaluate the combination regimen of rintodestrant and the CDK4/6 inhibitor Ibrance® (palbociclib). Palbociclib is being provided by Pfizer Inc. under a non-exclusive clinical supply agreement.
<a href="https://www.g1therapeutics.com/pipeline/rintodestrant/">Source</a>

G1 Therapeutics

Company Details