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

Primary targets: CHK1 · FDA status: FDA trials Discontinued after Phase II

Selectivity scorecard

MeasuredDerived
KISS
98.74
Gini
0.687
CATDS
0.025

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 Rabusertib. Strongest target: CHK1 at 99.4% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1CHK199.4%0.6%
2RAF195.6%4.4%
3CAMK2A92.0%8.0%
4RSK391.1%8.9%
5CAMK2D90.9%9.1%
6RSK484.3%15.8%
7CDK3_CYCLIN_C80.3%19.7%
8RSK276.2%23.8%
9TRKC75.2%24.8%
10RSK174.3%25.7%
11SIK272.1%27.9%
12FLT371.2%28.8%
13TNIK57.8%42.2%
14BRSK256.9%43.1%
15MEK553.9%46.1%
16AMPK(A2_B2_G2)48.0%52.0%
17LOK_STK1047.4%52.6%
18MSSK1_STK2344.1%55.9%
19AMPK(A2_B2_G1)41.9%58.1%
20BRAF41.1%58.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Rabusertib

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
1037.82
ALLOGRAFT_REJECTION
1753.24
ANDROGEN_RESPONSE
819.33
ANGIOGENESIS
323.73
APICAL_JUNCTION
2448.05
APICAL_SURFACE
159.13
APOPTOSIS
3096.42
BILE_ACID_METABOLISM
451.83
CHOLESTEROL_HOMEOSTASIS
386.09
COAGULATION
129.57
COMPLEMENT
1335.97
DNA_REPAIR
468.98
E2F_TARGETS
2513.30
EPITHELIAL_MESENCHYMAL_TRANSITION
1332.27
ESTROGEN_RESPONSE_EARLY
1907.59
ESTROGEN_RESPONSE_LATE
1437.23
FATTY_ACID_METABOLISM
239.25
G2M_CHECKPOINT
2143.87
GLYCOLYSIS
1188.30
HEDGEHOG_SIGNALING
367.82
HEME_METABOLISM
730.36
HYPOXIA
1510.91
IL2_STAT5_SIGNALING
715.96
IL6_JAK_STAT3_SIGNALING
880.63
INFLAMMATORY_RESPONSE
1617.41
INTERFERON_ALPHA_RESPONSE
239.45
INTERFERON_GAMMA_RESPONSE
1166.42
KRAS_SIGNALING_DN
841.67
KRAS_SIGNALING_UP
767.54
MITOTIC_SPINDLE
2266.07
MTORC1_SIGNALING
1432.00
MYC_TARGETS_V1
1342.06
MYC_TARGETS_V2
457.98
MYOGENESIS
1644.85
NOTCH_SIGNALING
147.38
OXIDATIVE_PHOSPHORYLATION
466.96
P53_PATHWAY
1254.14
PANCREAS_BETA_CELLS
112.05
PEROXISOME
722.16
PI3K_AKT_MTOR_SIGNALING
2893.43
PROTEIN_SECRETION
972.61
REACTIVE_OXYGEN_SPECIES_PATHWAY
85.69
SPERMATOGENESIS
644.24
TGF_BETA_SIGNALING
1006.15
TNFA_SIGNALING_VIA_NFKB
1888.87
UNFOLDED_PROTEIN_RESPONSE
739.05
UV_RESPONSE_DN
2080.22
UV_RESPONSE_UP
1359.14
WNT_BETA_CATENIN_SIGNALING
1297.29
XENOBIOTIC_METABOLISM
664.78

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 = 3.14 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 = 0.845

SampleCancer typecos to ideal
EPT0291EPN0.845
SRR233037520.829
TCGA-CF-A5U8-01A-11R-A28M-070.827
b6a7e87e-2674-4a48-a3c2-c8a9806762b50.817
aMVAC.P_005_TURBT_S2230.816

Annotations

Sign in to read and post annotations.

Loading…