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Table 2 Medicines which have the ability to overcome resistance to treatment in CML

From: The importance of personalized medicine in chronic myeloid leukemia management: a narrative review

Medicine name

Mechanism

Combination with TKIs or chemotherapies

References

Ruxolitinib

Inhibition of STAT-5 activity

Nilotinib

[246]

bardoxolone methyl (CDDO-Me)

Inhibition of STAT-3 activity

 

[247]

BP-5-087

Inhibition of STAT-3 activity

IMA

[248]

Everolimus (RAD001)

mTOR inhibitor

 

[177]

NVP-BEZ235

mTOR inhibitor

 

[249]

Pictilisib (GDC-0941)

PI3K inhibitor

Dastatinib

[179]

LY294002

PI3K inhibitor

IMA

[250, 251]

trametinib (GSK1120212)

MEK inhibitor

IMA

[181]

U0126

MEK inhibitor

Dastatinib/IMA

[252]

PD184352

MEK inhibitor

 

[253, 254]

Wortmannin

PI3K inhibitor

IMA

[255]

INNO-406

inhibit Pgp export pump

Cyclosporin A

[256]

MK-0457 (VX-680)

Aurora A, B and C kinase inhibitor

 

[257]

Tipifarnib (R115777)

Ras farnelysation inhibitor

IMA

[258,259,260]

Lonafarnib (SCH66336)

Ras farnelysation inhibitor

 

[261]

BMS-214662

Ras farnelysation inhibitor

 

[253]

17-allylamino-17-demethoxygeldanamycin

Pgp pump inhibitor and Hsp90 inhibitor

IMA

[262, 263]

  1. STAT, signal transducer and activator of transcription; mTOR, mammalian target of rapamycin; PI3K, phosphoinositide 3-kinase; MEK, mitogen-activated protein kinase kinase; Pgp, P-glycoprotein; Ras, rat sarcoma virus; Hsp90, heat shock protein 90