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

Primary targets: FAK_PTK2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
92.68
Gini
0.450
CATDS
0.006

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 Defactinib. Strongest target: ERBB4_HER4 at 99.6% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ERBB4_HER499.6%0.4%
2FAK_PTK298.5%1.5%
3CLK197.9%2.1%
4CDK5_P2596.8%3.2%
5MLK3_MAP3K1196.4%3.6%
6GSK3B96.3%3.7%
7CDK1_CYCLIN_A96.3%3.7%
8LRRK295.8%4.2%
9JAK295.3%4.7%
10MUSK95.2%4.8%
11TYK295.0%5.0%
12YSK4_MAP3K1994.9%5.1%
13EGFR94.6%5.4%
14FLT394.6%5.4%
15CLK294.5%5.5%
16CDK9_CYCLIN_K93.7%6.3%
17JAK193.7%6.3%
18CDK3_CYCLIN_E92.6%7.4%
19CDK2_CYCLIN_E92.6%7.4%
20MLK1_MAP3K992.2%7.8%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Defactinib

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
4408.84
ALLOGRAFT_REJECTION
10894.07
ANDROGEN_RESPONSE
3695.05
ANGIOGENESIS
1960.04
APICAL_JUNCTION
11837.48
APICAL_SURFACE
1412.41
APOPTOSIS
11785.74
BILE_ACID_METABOLISM
1469.06
CHOLESTEROL_HOMEOSTASIS
1877.38
COAGULATION
1352.35
COMPLEMENT
6749.19
DNA_REPAIR
3873.19
E2F_TARGETS
11204.86
EPITHELIAL_MESENCHYMAL_TRANSITION
3661.89
ESTROGEN_RESPONSE_EARLY
5832.69
ESTROGEN_RESPONSE_LATE
6187.83
FATTY_ACID_METABOLISM
1219.02
G2M_CHECKPOINT
11105.81
GLYCOLYSIS
4428.44
HEDGEHOG_SIGNALING
1738.03
HEME_METABOLISM
4130.32
HYPOXIA
6985.85
IL2_STAT5_SIGNALING
5346.03
IL6_JAK_STAT3_SIGNALING
8476.88
INFLAMMATORY_RESPONSE
7670.24
INTERFERON_ALPHA_RESPONSE
1491.24
INTERFERON_GAMMA_RESPONSE
10382.70
KRAS_SIGNALING_DN
1831.06
KRAS_SIGNALING_UP
5008.64
MITOTIC_SPINDLE
10394.90
MTORC1_SIGNALING
6260.85
MYC_TARGETS_V1
6748.85
MYC_TARGETS_V2
1718.00
MYOGENESIS
5639.54
NOTCH_SIGNALING
889.10
OXIDATIVE_PHOSPHORYLATION
1852.07
P53_PATHWAY
7248.86
PANCREAS_BETA_CELLS
1109.97
PEROXISOME
2064.04
PI3K_AKT_MTOR_SIGNALING
13083.60
PROTEIN_SECRETION
2796.07
REACTIVE_OXYGEN_SPECIES_PATHWAY
903.86
SPERMATOGENESIS
3017.94
TGF_BETA_SIGNALING
3865.30
TNFA_SIGNALING_VIA_NFKB
9056.80
UNFOLDED_PROTEIN_RESPONSE
3008.41
UV_RESPONSE_DN
7673.12
UV_RESPONSE_UP
5470.97
WNT_BETA_CATENIN_SIGNALING
4309.15
XENOBIOTIC_METABOLISM
2922.13

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 = 0.879

SampleCancer typecos to ideal
EPT0291EPN0.879
TCGA-CF-A5U8-01A-11R-A28M-070.864
SRR122024980.851
aMVAC.P_005_TURBT_S2230.846
SRR1443713GTEX0.846

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