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

Primary targets: ROS_ROS1 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
84.21
Gini
0.608
CATDS
0.008

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 Repotrectinib. Strongest target: ROS_ROS1 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ROS_ROS1100.0%0.0%
2TRKB99.8%0.2%
3TXK99.8%0.2%
4EPHA299.6%0.4%
5ALK99.4%0.6%
6BMX_ETK99.3%0.7%
7DDR199.3%0.7%
8FAK_PTK299.2%0.8%
9ACK199.0%1.0%
10TRKA98.9%1.1%
11TRKC98.9%1.1%
12FGR98.9%1.1%
13LYN98.7%1.3%
14MUSK98.6%1.4%
15LCK98.6%1.4%
16YES_YES198.4%1.6%
17BLK98.4%1.6%
18JAK298.3%1.7%
19DDR298.3%1.8%
20EPHB498.2%1.8%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Repotrectinib

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
3626.57
ALLOGRAFT_REJECTION
12956.21
ANDROGEN_RESPONSE
2075.73
ANGIOGENESIS
2134.74
APICAL_JUNCTION
12335.68
APICAL_SURFACE
1313.64
APOPTOSIS
9337.04
BILE_ACID_METABOLISM
1311.23
CHOLESTEROL_HOMEOSTASIS
1607.44
COAGULATION
1584.94
COMPLEMENT
7491.81
DNA_REPAIR
2023.81
E2F_TARGETS
5678.90
EPITHELIAL_MESENCHYMAL_TRANSITION
2897.40
ESTROGEN_RESPONSE_EARLY
5213.04
ESTROGEN_RESPONSE_LATE
4516.06
FATTY_ACID_METABOLISM
941.37
G2M_CHECKPOINT
5826.44
GLYCOLYSIS
3968.07
HEDGEHOG_SIGNALING
1254.23
HEME_METABOLISM
2719.76
HYPOXIA
5193.94
IL2_STAT5_SIGNALING
4490.33
IL6_JAK_STAT3_SIGNALING
7921.83
INFLAMMATORY_RESPONSE
7020.04
INTERFERON_ALPHA_RESPONSE
1192.07
INTERFERON_GAMMA_RESPONSE
8612.79
KRAS_SIGNALING_DN
1577.31
KRAS_SIGNALING_UP
4339.81
MITOTIC_SPINDLE
8174.52
MTORC1_SIGNALING
4809.31
MYC_TARGETS_V1
3636.93
MYC_TARGETS_V2
982.60
MYOGENESIS
4680.26
NOTCH_SIGNALING
143.46
OXIDATIVE_PHOSPHORYLATION
1484.66
P53_PATHWAY
4480.50
PANCREAS_BETA_CELLS
322.15
PEROXISOME
1598.59
PI3K_AKT_MTOR_SIGNALING
12071.37
PROTEIN_SECRETION
2778.59
REACTIVE_OXYGEN_SPECIES_PATHWAY
564.41
SPERMATOGENESIS
1918.76
TGF_BETA_SIGNALING
2395.82
TNFA_SIGNALING_VIA_NFKB
5541.63
UNFOLDED_PROTEIN_RESPONSE
1895.53
UV_RESPONSE_DN
6601.26
UV_RESPONSE_UP
5296.58
WNT_BETA_CATENIN_SIGNALING
2579.75
XENOBIOTIC_METABOLISM
2659.38

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 = 0.832

SampleCancer typecos to ideal
EPT0291EPN0.832
SRR233037520.831
SRR108999840.820
TCGA-CF-A5U8-01A-11R-A28M-070.817
aMVAC.P_005_TURBT_S2230.814

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