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Chronic Myeloid Leukemia (CML)

Chronic Myeloid Leukemia (CML) is a type of myeloproliferative neoplasm characterized by the presence of the Philadelphia chromosome (Ph), resulting from a reciprocal translocation between chromosomes 9 and 22. At our company, we are fully committed to offering comprehensive services for the development of drugs and therapies targeting CML.

What is Chronic Myeloid Leukemia (CML)?

Chronic Myeloid Leukemia (CML) is a rare blood cancer characterized by the excessive growth of myeloid cells within the bone marrow and bloodstream. It is estimated that approximately 1-1.5 individuals per 100,000 are diagnosed with CML annually, without significant racial or geographic differences. The disease progresses through three distinct phases: chronic phase (CP), accelerated phase (AP), and blast phase (BP). The majority of CML cases are diagnosed in the chronic phase, which is characterized by an expansion of functionally normal myeloid cells.

2-1-12-2-1-1 Chronic Myeloid Leukemia (CML)-1Fig.1 Modulation of tyrosine kinase inhibitors (TKIs) in CML. (Hsieh, Y.C., et al., 2021)

Pathogenesis of Chronic Myeloid Leukemia (CML)

The defining characteristic of Chronic Myeloid Leukemia (CML) is the presence of the BCR-ABL1 fusion gene, which arises from a reciprocal translocation between chromosomes 9 and 22 [t (9; 22) (q34; q11.2)]. This genetic anomaly gives rise to the BCR-ABL1 fusion protein, which exhibits constitutive tyrosine kinase activity. The dysregulated kinase activity of BCR-ABL1 triggers the activation of various signaling pathways involved in cell proliferation, survival, and differentiation.

These signaling pathways include the phosphatidylinositol-3 kinase (PI3K) pathway, the RAS/mitogen-activated protein kinase (MAPK) pathway, and the Janus kinase (JAK)/Signal transducer and activator of transcription (STAT) pathways, among others. Activation of these pathways facilitates the growth of leukemic cells, inhibits programmed cell death (apoptosis), and disrupts normal cellular functions.

Targeted Therapy Development for CML

In the process of developing effective drugs and therapies for CML, targeting the BCR-ABL1 fusion protein and its downstream signaling pathways is the main direction. The development of tyrosine kinase inhibitors (TKI) is a revolutionary change in the development of CML therapies. TKIs such as imatinib, dasatinib, and nilotinib have shown remarkable efficacy in inducing deep molecular responses and prolonging overall survival in CML. However, resistance to TKI is also the most challenging problem in CML targeted therapy.

Our Services

With a team of highly skilled and experienced biological experts who have worked in the industry for many years, our company understands the unique challenges associated with CML therapy and is committed to providing cutting-edge solutions. We have developed a profound understanding of the molecular mechanisms of CML and have conducted extensive research in this field. Our expertise allows us to provide CML diagnostics development and innovative therapy development to pharmaceutical companies worldwide.

Our CML Therapy Development Platforms

At our company, we have established robust animal models of CML to study disease progression and evaluate the pharmacokinetics and drug safety of novel drug candidates. By utilizing these models, we can gain valuable insights into the mechanisms underlying CML and optimize therapeutic interventions before moving into clinical trials.

When you choose our company for chronic myeloid leukemia (CML) drug and therapy development services, you can be confident that you are partnering with a trusted and experienced team.

CML Animal Model Development Service

  • Conventional transgenic models
  • Xenograft nude mice injected with K562
  • Xenograft SCID mice
  • Xenograft NOD/SCID models

If you are interested in our services, please feel free to contact us for more details and quotation information of related services.

References

  • Hsieh, Y.C., et al., "Improving outcomes in chronic myeloid leukemia through harnessing the immunological landscape." Leukemia 35.5 (2021): 1229-1242.
  • Osman, Afaf EG, and Michael W. Deininger. "Chronic Myeloid Leukemia: Modern therapies, current challenges, and future directions." Blood reviews 49 (2021): 100825.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

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