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

Primary targets: SYK · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
96.74
Gini
0.613
CATDS
0.011

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 Fostamatinib. Strongest target: NEK9 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1NEK9100.0%0.0%
2EGFR97.8%2.2%
3FLT397.2%2.8%
4AURORA_A97.0%3.0%
5ROS_ROS195.8%4.2%
6MLK2_MAP3K1094.2%5.8%
7EPHA192.8%7.2%
8EPHA491.5%8.5%
9MUSK90.8%9.3%
10JAK290.6%9.4%
11EPHB190.2%9.8%
12RET90.1%9.9%
13AURORA_C90.0%10.0%
14EPHA688.3%11.7%
15EPHA287.9%12.1%
16FLT4_VEGFR387.2%12.8%
17ERBB2_HER287.0%13.0%
18MLK1_MAP3K985.4%14.6%
19MLK3_MAP3K1185.1%14.9%
20PYK284.9%15.1%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Fostamatinib

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-target2%
Off-target98%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
2919.92
ALLOGRAFT_REJECTION
9223.40
ANDROGEN_RESPONSE
2224.27
ANGIOGENESIS
1847.65
APICAL_JUNCTION
10546.21
APICAL_SURFACE
1125.92
APOPTOSIS
6959.66
BILE_ACID_METABOLISM
1156.91
CHOLESTEROL_HOMEOSTASIS
1404.69
COAGULATION
1113.70
COMPLEMENT
5622.44
DNA_REPAIR
1802.94
E2F_TARGETS
4797.10
EPITHELIAL_MESENCHYMAL_TRANSITION
2192.74
ESTROGEN_RESPONSE_EARLY
3142.73
ESTROGEN_RESPONSE_LATE
3045.35
FATTY_ACID_METABOLISM
991.64
G2M_CHECKPOINT
4875.04
GLYCOLYSIS
2836.26
HEDGEHOG_SIGNALING
1168.88
HEME_METABOLISM
2168.54
HYPOXIA
4260.18
IL2_STAT5_SIGNALING
3365.67
IL6_JAK_STAT3_SIGNALING
6212.96
INFLAMMATORY_RESPONSE
5643.63
INTERFERON_ALPHA_RESPONSE
1003.41
INTERFERON_GAMMA_RESPONSE
7050.71
KRAS_SIGNALING_DN
935.11
KRAS_SIGNALING_UP
3775.48
MITOTIC_SPINDLE
6842.06
MTORC1_SIGNALING
3993.84
MYC_TARGETS_V1
3372.69
MYC_TARGETS_V2
827.25
MYOGENESIS
3329.50
NOTCH_SIGNALING
284.96
OXIDATIVE_PHOSPHORYLATION
1646.96
P53_PATHWAY
3536.73
PANCREAS_BETA_CELLS
245.73
PEROXISOME
959.41
PI3K_AKT_MTOR_SIGNALING
9449.00
PROTEIN_SECRETION
2060.42
REACTIVE_OXYGEN_SPECIES_PATHWAY
442.13
SPERMATOGENESIS
1669.75
TGF_BETA_SIGNALING
1759.70
TNFA_SIGNALING_VIA_NFKB
4796.34
UNFOLDED_PROTEIN_RESPONSE
1645.71
UV_RESPONSE_DN
5012.15
UV_RESPONSE_UP
3582.28
WNT_BETA_CATENIN_SIGNALING
2073.08
XENOBIOTIC_METABOLISM
2220.16

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 = 3.09 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 = 0.839

SampleCancer typecos to ideal
EPT0291EPN0.839
SRR233037520.837
TCGA-CF-A5U8-01A-11R-A28M-070.829
SRR108999840.825
TCGA-FD-A43X-01A-11R-A23W-070.825

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