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

Primary targets: TRKA, TRKB, TRKC · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.25
Gini
0.710
CATDS
0.047

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 Larotrectinib. Strongest target: TRKA at 98.5% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1TRKA98.5%1.5%
2TRKC98.1%1.9%
3TRKB97.9%2.1%
4ROS_ROS189.5%10.5%
5ACK157.8%42.2%
6MUSK52.5%47.5%
7DDR151.2%48.8%
8DDR243.7%56.3%
9LIMK132.8%67.2%
10TXK29.6%70.4%
11ARK5_NUAK125.7%74.3%
12BMX_ETK25.3%74.7%
13TYK1_LTK20.5%79.5%
14JAK220.3%79.7%
15GRK619.2%80.8%
16MST3_STK2419.0%81.0%
17MLCK2_MYLK218.7%81.3%
18CK2A218.6%81.4%
19C_MET17.4%82.6%
20PDK2_PDHK216.7%83.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Larotrectinib

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
433.25
ALLOGRAFT_REJECTION
1098.03
ANDROGEN_RESPONSE
332.96
ANGIOGENESIS
197.44
APICAL_JUNCTION
1228.55
APICAL_SURFACE
156.34
APOPTOSIS
1230.82
BILE_ACID_METABOLISM
153.00
CHOLESTEROL_HOMEOSTASIS
248.57
COAGULATION
193.07
COMPLEMENT
856.46
DNA_REPAIR
303.53
E2F_TARGETS
914.29
EPITHELIAL_MESENCHYMAL_TRANSITION
354.32
ESTROGEN_RESPONSE_EARLY
574.46
ESTROGEN_RESPONSE_LATE
500.04
FATTY_ACID_METABOLISM
115.22
G2M_CHECKPOINT
903.64
GLYCOLYSIS
443.15
HEDGEHOG_SIGNALING
149.71
HEME_METABOLISM
364.81
HYPOXIA
701.62
IL2_STAT5_SIGNALING
495.78
IL6_JAK_STAT3_SIGNALING
787.81
INFLAMMATORY_RESPONSE
740.03
INTERFERON_ALPHA_RESPONSE
102.14
INTERFERON_GAMMA_RESPONSE
754.58
KRAS_SIGNALING_DN
189.19
KRAS_SIGNALING_UP
499.82
MITOTIC_SPINDLE
1090.22
MTORC1_SIGNALING
612.37
MYC_TARGETS_V1
609.93
MYC_TARGETS_V2
123.64
MYOGENESIS
541.95
NOTCH_SIGNALING
63.78
OXIDATIVE_PHOSPHORYLATION
241.65
P53_PATHWAY
525.26
PANCREAS_BETA_CELLS
49.07
PEROXISOME
178.38
PI3K_AKT_MTOR_SIGNALING
1409.37
PROTEIN_SECRETION
316.76
REACTIVE_OXYGEN_SPECIES_PATHWAY
87.69
SPERMATOGENESIS
333.29
TGF_BETA_SIGNALING
320.19
TNFA_SIGNALING_VIA_NFKB
688.39
UNFOLDED_PROTEIN_RESPONSE
245.44
UV_RESPONSE_DN
750.09
UV_RESPONSE_UP
759.90
WNT_BETA_CATENIN_SIGNALING
363.67
XENOBIOTIC_METABOLISM
270.83

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 = 3.12 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 = 0.863

SampleCancer typecos to ideal
EPT0291EPN0.863
SRR233037520.849
TCGA-CF-A5U8-01A-11R-A28M-070.846
SRR122024980.838
TCGA-FD-A43X-01A-11R-A23W-070.833

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