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

Primary targets: RET · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
93.43
Gini
0.643
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 Pralsetinib. Strongest target: RET at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1RET100.0%0.0%
2ERBB4_HER499.7%0.3%
3TRKC99.4%0.6%
4TRKB99.4%0.6%
5EGFR99.1%0.9%
6JAK199.1%0.9%
7JAK299.1%0.9%
8TRKA98.7%1.3%
9JAK398.1%1.9%
10FLT397.6%2.4%
11ERBB2_HER297.5%2.5%
12ROS_ROS197.3%2.7%
13DDR196.9%3.1%
14TYK296.8%3.2%
15MLK3_MAP3K1196.5%3.5%
16FLT4_VEGFR396.5%3.5%
17LIMK196.4%3.6%
18BLK96.1%3.9%
19DDR295.9%4.1%
20C_KIT93.8%6.2%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Pralsetinib

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-target1%
Off-target99%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
3617.60
ALLOGRAFT_REJECTION
10878.12
ANDROGEN_RESPONSE
2594.93
ANGIOGENESIS
1755.61
APICAL_JUNCTION
11094.57
APICAL_SURFACE
1090.24
APOPTOSIS
7953.98
BILE_ACID_METABOLISM
1078.77
CHOLESTEROL_HOMEOSTASIS
1737.81
COAGULATION
1300.49
COMPLEMENT
6585.18
DNA_REPAIR
2305.52
E2F_TARGETS
5462.02
EPITHELIAL_MESENCHYMAL_TRANSITION
2732.20
ESTROGEN_RESPONSE_EARLY
3580.18
ESTROGEN_RESPONSE_LATE
3488.19
FATTY_ACID_METABOLISM
1139.76
G2M_CHECKPOINT
5892.44
GLYCOLYSIS
3187.60
HEDGEHOG_SIGNALING
1003.38
HEME_METABOLISM
2613.11
HYPOXIA
4593.44
IL2_STAT5_SIGNALING
4064.15
IL6_JAK_STAT3_SIGNALING
8317.58
INFLAMMATORY_RESPONSE
6604.15
INTERFERON_ALPHA_RESPONSE
1256.38
INTERFERON_GAMMA_RESPONSE
8788.05
KRAS_SIGNALING_DN
945.16
KRAS_SIGNALING_UP
4398.07
MITOTIC_SPINDLE
7638.67
MTORC1_SIGNALING
4372.69
MYC_TARGETS_V1
3895.39
MYC_TARGETS_V2
910.11
MYOGENESIS
3489.46
NOTCH_SIGNALING
359.35
OXIDATIVE_PHOSPHORYLATION
1863.05
P53_PATHWAY
4110.22
PANCREAS_BETA_CELLS
372.74
PEROXISOME
1487.22
PI3K_AKT_MTOR_SIGNALING
11204.68
PROTEIN_SECRETION
2255.39
REACTIVE_OXYGEN_SPECIES_PATHWAY
710.62
SPERMATOGENESIS
1788.71
TGF_BETA_SIGNALING
2369.43
TNFA_SIGNALING_VIA_NFKB
6133.14
UNFOLDED_PROTEIN_RESPONSE
1812.68
UV_RESPONSE_DN
5683.17
UV_RESPONSE_UP
4081.25
WNT_BETA_CATENIN_SIGNALING
2293.95
XENOBIOTIC_METABOLISM
2249.07

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 = 3.07 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 = 0.847

SampleCancer typecos to ideal
EPT0291EPN0.847
SRR233037520.840
SRR108999840.836
TCGA-CF-A5U8-01A-11R-A28M-070.833
aMVAC.P_005_TURBT_S2230.830

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