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

Primary targets: JAK2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
88.64
Gini
0.452
CATDS
0.006

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 Pacritinib. Strongest target: IRAK1 at 99.6% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1IRAK199.6%0.4%
2TNIK99.2%0.8%
3CLK198.8%1.2%
4TYK298.8%1.2%
5JAK298.4%1.6%
6LCK98.4%1.6%
7C_KIT98.4%1.6%
8ROS_ROS198.2%1.8%
9CDK9_CYCLIN_K98.0%2.0%
10CDK9_CYCLIN_T297.9%2.1%
11HIPK297.4%2.6%
12HGK_MAP4K497.1%2.9%
13ALK1_ACVRL196.9%3.1%
14CDK9_CYCLIN_T196.8%3.2%
15TRKC96.7%3.3%
16ALK2_ACVR196.7%3.4%
17PKCA96.4%3.6%
18HIPK496.2%3.8%
19FMS95.7%4.3%
20MINK_MINK195.1%4.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Pacritinib

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-target3%
Off-target97%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
4851.64
ALLOGRAFT_REJECTION
14371.56
ANDROGEN_RESPONSE
4173.82
ANGIOGENESIS
2307.11
APICAL_JUNCTION
14860.79
APICAL_SURFACE
1581.67
APOPTOSIS
12645.29
BILE_ACID_METABOLISM
1649.04
CHOLESTEROL_HOMEOSTASIS
2228.77
COAGULATION
1647.62
COMPLEMENT
8829.61
DNA_REPAIR
3713.83
E2F_TARGETS
10128.84
EPITHELIAL_MESENCHYMAL_TRANSITION
4472.97
ESTROGEN_RESPONSE_EARLY
6638.17
ESTROGEN_RESPONSE_LATE
6380.69
FATTY_ACID_METABOLISM
1330.16
G2M_CHECKPOINT
10140.65
GLYCOLYSIS
4863.90
HEDGEHOG_SIGNALING
2050.13
HEME_METABOLISM
4080.32
HYPOXIA
7385.59
IL2_STAT5_SIGNALING
5737.96
IL6_JAK_STAT3_SIGNALING
9789.13
INFLAMMATORY_RESPONSE
8948.16
INTERFERON_ALPHA_RESPONSE
1635.96
INTERFERON_GAMMA_RESPONSE
11858.98
KRAS_SIGNALING_DN
2181.49
KRAS_SIGNALING_UP
5785.78
MITOTIC_SPINDLE
11375.45
MTORC1_SIGNALING
6781.58
MYC_TARGETS_V1
6801.57
MYC_TARGETS_V2
1568.74
MYOGENESIS
6236.04
NOTCH_SIGNALING
781.00
OXIDATIVE_PHOSPHORYLATION
2031.90
P53_PATHWAY
7518.13
PANCREAS_BETA_CELLS
1015.98
PEROXISOME
2357.18
PI3K_AKT_MTOR_SIGNALING
15445.48
PROTEIN_SECRETION
3373.59
REACTIVE_OXYGEN_SPECIES_PATHWAY
928.83
SPERMATOGENESIS
3192.56
TGF_BETA_SIGNALING
4091.11
TNFA_SIGNALING_VIA_NFKB
9364.18
UNFOLDED_PROTEIN_RESPONSE
3134.68
UV_RESPONSE_DN
8913.18
UV_RESPONSE_UP
6912.42
WNT_BETA_CATENIN_SIGNALING
4325.51
XENOBIOTIC_METABOLISM
3544.81

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-070.849
SRR233037520.846
SRR122024980.842
aMVAC.P_005_TURBT_S2230.841

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