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

Primary targets: PI3K · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
100.00
Gini
0.716
CATDS
0.030

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 Duvelisib. Strongest target: PDK2_PDHK2 at 42.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1PDK2_PDHK242.7%57.3%
2CAMKK234.4%65.6%
3DNA_PK33.4%66.6%
4PKG2_PRKG233.3%66.7%
5VRK124.2%75.8%
6P38A_MAPK1421.9%78.1%
7LYN21.7%78.3%
8STK39_STLK321.6%78.4%
9PKMYT120.3%79.7%
10GSK3A18.7%81.3%
11AURORA_C18.6%81.4%
12HASPIN18.5%81.5%
13CDK2_CYCLIN_A118.2%81.8%
14MUSK18.2%81.8%
15MEKK317.6%82.4%
16ITK17.5%82.5%
17ROS_ROS116.5%83.5%
18EPHA415.8%84.2%
19PKCTHETA15.4%84.6%
20PDK1_PDPK115.2%84.8%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Duvelisib

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
386.31
ALLOGRAFT_REJECTION
1092.41
ANDROGEN_RESPONSE
404.22
ANGIOGENESIS
150.25
APICAL_JUNCTION
1103.04
APICAL_SURFACE
111.54
APOPTOSIS
1127.79
BILE_ACID_METABOLISM
158.09
CHOLESTEROL_HOMEOSTASIS
148.83
COAGULATION
120.06
COMPLEMENT
592.74
DNA_REPAIR
338.79
E2F_TARGETS
1029.36
EPITHELIAL_MESENCHYMAL_TRANSITION
352.61
ESTROGEN_RESPONSE_EARLY
458.97
ESTROGEN_RESPONSE_LATE
463.57
FATTY_ACID_METABOLISM
153.59
G2M_CHECKPOINT
881.47
GLYCOLYSIS
419.10
HEDGEHOG_SIGNALING
113.08
HEME_METABOLISM
333.17
HYPOXIA
646.13
IL2_STAT5_SIGNALING
463.67
IL6_JAK_STAT3_SIGNALING
640.07
INFLAMMATORY_RESPONSE
693.80
INTERFERON_ALPHA_RESPONSE
140.52
INTERFERON_GAMMA_RESPONSE
863.75
KRAS_SIGNALING_DN
180.33
KRAS_SIGNALING_UP
475.99
MITOTIC_SPINDLE
871.96
MTORC1_SIGNALING
547.86
MYC_TARGETS_V1
686.23
MYC_TARGETS_V2
212.09
MYOGENESIS
463.28
NOTCH_SIGNALING
78.84
OXIDATIVE_PHOSPHORYLATION
143.45
P53_PATHWAY
648.03
PANCREAS_BETA_CELLS
71.94
PEROXISOME
158.46
PI3K_AKT_MTOR_SIGNALING
1327.24
PROTEIN_SECRETION
244.22
REACTIVE_OXYGEN_SPECIES_PATHWAY
45.66
SPERMATOGENESIS
409.07
TGF_BETA_SIGNALING
294.21
TNFA_SIGNALING_VIA_NFKB
768.71
UNFOLDED_PROTEIN_RESPONSE
256.36
UV_RESPONSE_DN
580.02
UV_RESPONSE_UP
500.19
WNT_BETA_CATENIN_SIGNALING
347.64
XENOBIOTIC_METABOLISM
281.86

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 = 0.867

SampleCancer typecos to ideal
EPT0291EPN0.867
TCGA-CF-A5U8-01A-11R-A28M-070.854
SRR122024980.840
SRR1443713GTEX0.835
C3N-034200.834

Annotations

Sign in to read and post annotations.

Loading…