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
88.97
Gini
0.506
CATDS
0.007

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 Gilteritinib. Strongest target: RET at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1RET100.0%0.0%
2TYK1_LTK99.7%0.3%
3ROS_ROS199.6%0.4%
4ALK99.5%0.5%
5FLT399.2%0.8%
6TRKC99.0%1.0%
7TNIK98.8%1.2%
8AXL98.7%1.3%
9FLT4_VEGFR398.5%1.5%
10C_MER98.4%1.6%
11LOK_STK1098.3%1.7%
12MLK3_MAP3K1197.4%2.6%
13LRRK297.2%2.8%
14STK22D_TSSK196.8%3.2%
15DDR296.7%3.3%
16BRK96.6%3.4%
17HPK1_MAP4K196.6%3.4%
18FGR95.8%4.2%
19DDR195.7%4.3%
20MINK_MINK195.7%4.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Gilteritinib

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-target0%
Off-target100%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
3664.21
ALLOGRAFT_REJECTION
13029.26
ANDROGEN_RESPONSE
2998.28
ANGIOGENESIS
2332.46
APICAL_JUNCTION
13769.90
APICAL_SURFACE
1361.08
APOPTOSIS
9591.22
BILE_ACID_METABOLISM
1394.29
CHOLESTEROL_HOMEOSTASIS
1894.57
COAGULATION
1534.25
COMPLEMENT
7813.82
DNA_REPAIR
2783.93
E2F_TARGETS
6803.45
EPITHELIAL_MESENCHYMAL_TRANSITION
3241.14
ESTROGEN_RESPONSE_EARLY
4856.85
ESTROGEN_RESPONSE_LATE
4486.52
FATTY_ACID_METABOLISM
1127.12
G2M_CHECKPOINT
6729.63
GLYCOLYSIS
4128.09
HEDGEHOG_SIGNALING
1630.81
HEME_METABOLISM
2832.71
HYPOXIA
5607.72
IL2_STAT5_SIGNALING
4227.49
IL6_JAK_STAT3_SIGNALING
7985.80
INFLAMMATORY_RESPONSE
7288.40
INTERFERON_ALPHA_RESPONSE
1106.85
INTERFERON_GAMMA_RESPONSE
9390.61
KRAS_SIGNALING_DN
1603.41
KRAS_SIGNALING_UP
5046.30
MITOTIC_SPINDLE
9082.70
MTORC1_SIGNALING
5331.62
MYC_TARGETS_V1
4706.14
MYC_TARGETS_V2
1126.54
MYOGENESIS
4608.98
NOTCH_SIGNALING
461.88
OXIDATIVE_PHOSPHORYLATION
1848.69
P53_PATHWAY
4949.87
PANCREAS_BETA_CELLS
415.18
PEROXISOME
1623.67
PI3K_AKT_MTOR_SIGNALING
12612.95
PROTEIN_SECRETION
2965.66
REACTIVE_OXYGEN_SPECIES_PATHWAY
687.17
SPERMATOGENESIS
2155.71
TGF_BETA_SIGNALING
2757.18
TNFA_SIGNALING_VIA_NFKB
6240.22
UNFOLDED_PROTEIN_RESPONSE
2406.31
UV_RESPONSE_DN
7197.65
UV_RESPONSE_UP
5589.43
WNT_BETA_CATENIN_SIGNALING
3129.95
XENOBIOTIC_METABOLISM
2949.66

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 = 3.11 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 = 0.844

SampleCancer typecos to ideal
EPT0291EPN0.844
SRR233037520.837
TCGA-CF-A5U8-01A-11R-A28M-070.830
aMVAC.P_005_TURBT_S2230.826
SRR108999840.824

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