Research Use Only. KIRhub outputs are computational research artifacts. They are not validated for clinical decision-making, diagnosis, or treatment.

Primary targets: FLT3 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.50
Gini
0.737
CATDS
0.038

Computed from wild-type kinome inhibition at 1 μM. Gini reproduces the published values within tolerance; KISS and CATDS are computed but pending reconciliation with the paper's reference code.

Polypharmacology radar

MeasuredDerived

Top 20 strongest-inhibited wild-type kinases for Quizartinib. Strongest target: FLT3 at 97.9% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1FLT397.9%2.1%
2C_KIT97.3%2.7%
3PDGFRB89.0%11.0%
4FMS83.7%16.3%
5RET79.5%20.5%
6MUSK79.2%20.8%
7PDGFRA69.8%30.3%
8TRKB57.6%42.4%
9TRKC53.9%46.1%
10HIPK453.1%46.9%
11RIPK451.4%48.6%
12DDR148.2%51.8%
13ERK7_MAPK1544.3%55.7%
14KHS_MAP4K541.4%58.6%
15TRKA39.4%60.6%
16DDR238.5%61.5%
17FLT4_VEGFR336.3%63.7%
18CAMKK134.7%65.3%
19HGK_MAP4K433.3%66.7%
20MYLK324.5%75.5%

Selectivity landscape

MeasuredDerived

Where Quizartinib sits in the 92-drug selectivity landscape (KISS vs Gini). The highlighted point is Quizartinib.

Atlas insights for Quizartinib

MeasuredReference

Pathway-space view of what this drug actually does, drawn from the Pathway Atlas.

On-target vs off-target shadow

DerivedMeasured

How much of this drug's pathway perturbation comes from primary targets vs polypharmacology vs 2nd-order propagation. When off-target dominates, the FDA label is the smallest description of the drug.

On-target10%
Off-target90%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
577.29
ALLOGRAFT_REJECTION
1593.55
ANDROGEN_RESPONSE
461.67
ANGIOGENESIS
419.60
APICAL_JUNCTION
2544.76
APICAL_SURFACE
232.13
APOPTOSIS
2032.49
BILE_ACID_METABOLISM
348.87
CHOLESTEROL_HOMEOSTASIS
343.76
COAGULATION
209.22
COMPLEMENT
960.61
DNA_REPAIR
480.72
E2F_TARGETS
1571.46
EPITHELIAL_MESENCHYMAL_TRANSITION
521.71
ESTROGEN_RESPONSE_EARLY
908.23
ESTROGEN_RESPONSE_LATE
864.68
FATTY_ACID_METABOLISM
267.40
G2M_CHECKPOINT
1670.36
GLYCOLYSIS
668.50
HEDGEHOG_SIGNALING
445.08
HEME_METABOLISM
557.43
HYPOXIA
1089.20
IL2_STAT5_SIGNALING
705.19
IL6_JAK_STAT3_SIGNALING
917.09
INFLAMMATORY_RESPONSE
661.85
INTERFERON_ALPHA_RESPONSE
138.67
INTERFERON_GAMMA_RESPONSE
1031.51
KRAS_SIGNALING_DN
322.05
KRAS_SIGNALING_UP
770.16
MITOTIC_SPINDLE
1665.38
MTORC1_SIGNALING
891.16
MYC_TARGETS_V1
744.80
MYC_TARGETS_V2
232.84
MYOGENESIS
975.64
NOTCH_SIGNALING
95.87
OXIDATIVE_PHOSPHORYLATION
573.11
P53_PATHWAY
808.15
PANCREAS_BETA_CELLS
115.98
PEROXISOME
382.93
PI3K_AKT_MTOR_SIGNALING
2147.63
PROTEIN_SECRETION
362.56
REACTIVE_OXYGEN_SPECIES_PATHWAY
98.62
SPERMATOGENESIS
403.08
TGF_BETA_SIGNALING
525.63
TNFA_SIGNALING_VIA_NFKB
940.09
UNFOLDED_PROTEIN_RESPONSE
625.32
UV_RESPONSE_DN
1439.66
UV_RESPONSE_UP
752.55
WNT_BETA_CATENIN_SIGNALING
803.24
XENOBIOTIC_METABOLISM
435.93

See this drug on the perturbation map →

Hallmarks-of-Cancer reach

DerivedReference

Projection onto the 10 canonical Hanahan & Weinberg hallmarks. Breadth = how many hallmarks this drug meaningfully perturbs.

ProliferationEvading apoptosisAngiogenesisInvasion / metastasisReplicative immortalityDeregulated metabolismImmune evasionGenome instabilityInflammationGrowth signaling

Breadth = 3.17 bits (max possible across 10 hallmarks = 3.32 bits). Multi-hallmark agent — broad polypharmacology.

Compare against the full catalog →

Anti-tumor matches — the "ideal patient" search

ModeledDerived

Top 5 real tumors closest to this drug's ideal patient (the tumor whose pathway state = −Π_d). Closest match cosine = 0.827

SampleCancer typecos to ideal
EPT0291EPN0.827
SRR233037520.817
TCGA-CF-A5U8-01A-11R-A28M-070.815
aMVAC.P_005_TURBT_S2230.806
SRR122024980.800

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