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Fig. 1 · Structure
Cat. No.
A15554
CAS No.
1204669-58-8
Alternate CAS
1204669-37-3
Formula
C11H13BrFN7O4S
Mol. Weight
438.23

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Epacadostat (INCB024360)

Cat. No. A15554 CAS 1204669-58-8

IDO inhibitor

Epacadostat is a potent and selective indoleamine 2,3-dioxygenase (IDO1) inhibitor with IC50 of 10 nM, Phase 2,

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Publications for Epacadostat

3 publications citing this product

  1. Chunbo He, .et al. , Cancer Discov, 2024, Jan 12;14(1):176-193 PMID: 37931287
  2. Saeko Yoshioka, .et al. , Int J Tryptophan Res, 2022, Nov 30;15 PMID: 36467776
  3. Marta Galan-Diez, .et al. , Cancer Discov, 2022, Apr 1;12(4):1106-1127 PMID: 35046097
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Biological Activity

Bioactivity / Mechanism

Epacadostat inhibits IDO1-dependent kynurenine production. In a recombinant-enzyme comparison, its rhIDO1 IC50 was 0.01 μM (SE = ±0.0009), while the reported rhTDO IC50 was >1 μM. These assay-specific values do not establish a fixed selectivity ratio across biological systems. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
IDO1 10 nM

Cellular Effect

Cell Line Activity Value Description Reference
A549 IC50 > 100 μM Antiproliferative activity against human A549 cells after 48 hrs by CCK-8 assay [PMID: 29670692]
CT26 IC50 > 100 μM Antiproliferative activity against mouse CT26 cells after 48 hrs by CCK-8 assay [PMID: 29670692]
CT26 IC50 > 100 μM Cytotoxicity against mouse CT26 cells assessed as reduction in cell viability measured after 72 hrs by CCK8 assay [PMID: 33482599]
CT26 IC50 47.09 μM Cytotoxicity against mouse CT26 cells assessed as reduction in cell viability by CCK8 assay [PMID: 34854662]
HCT-116 IC50 > 100 μM Antiproliferative activity against human HCT116 cells after 48 hrs by CCK-8 assay [PMID: 29670692]
HCT-116 IC50 > 50 μM Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability measured after 72 hrs by MTT assay [PMID: 34147748]
HCT-116 IC50 37.1 μM Cytotoxicity against human HCT-116 cells assessed as reduction in cell viability by CCK8 assay [PMID: 34854662]
HEK293 IC50 0.242 μM Inhibition of TDO (unknown origin) expressed in HEK293 cells using L-Trp as substrate after 8 hrs [PMID: 30321802]
HEK293 IC50 0.26 μM Inhibition of human TDO transfected in HEK293 cells assessed as reduction in kynurenine production using L-tryptophan as substrate incubated for 12 hrs [PMID: 31580660]
HEK293 IC50 12.6 nM Inhibition of recombinant human IDO1 expressed in HEK293 cells assessed as N-formylkynurenine formation by measuring kynurenine level incubated for 12 hrs by microplate reader analysis [PMID: 31233921]
HeLa IC50 > 100 μM Cytotoxicity against human HeLa cells assessed as reduction in cell viability measured after 72 hrs by CCK8 assay [PMID: 33482599]
HeLa IC50 0.007 μM Inhibition of IDO1 in IFN-gamma stimulated human HeLa cells assessed as reduction in kynurenine production incubated for 18 hrs [PMID: 31580660]
HeLa IC50 0.016 μM Inhibition of IDO1 in IFN-gamma stimulated human HeLa cells assessed as reduction in kynurenine production using L-tryptophan as substrate incubated for 24 hrs [PMID: 31610376]
HeLa IC50 0.07 μM Inhibition of IDO1 in human HeLa cells using L-tryptophan as substrate after 20 hrs [PMID: 30469041]
HeLa IC50 10 nM Inhibition of IDO1 in human HeLa cells using L-tryptophan as substrate incubated for 48 hrs [PMID: 31445231]
HeLa IC50 10.3 nM Inhibition of IDO1 in IFN-gamma stimulated human HeLa cells assessed as reduction in kynurenine production incubated for 24 hrs relative to control [PMID: 30858027]
HeLa IC50 12.5 nM Inhibition of IDO1 in IFN-gamma stimulated human HeLa cells using L-tryptophan as substrate incubated for 48 hrs by fluorescence assay [PMID: 32832022]
HeLa IC50 7.1 nM Inhibition of IFN-gamma-stimulated IDO1 activity in human HeLa cells using L-tryptophan as substrate after 48 hrs by microplate reader analysis [PMID: 25970480]
HeLa IC50 7.1 nM Inhibition of IFN-gamma stimulated IDO1 in human HeLa cells assessed as reduction in formation of kynurenine incubated for 48 hrs in presence of IFNgamma by microplate reader assay [PMID: 31580660]

19 records · Scroll to view more

In Vitro Studies

In IFN-γ-stimulated A172 glioblastoma cells expressing IDO1 and TDO, epacadostat reduced kynurenine production without a comparable decrease in the viability signal. PVZB3001 produced stronger kynurenine suppression at ≥3 μM in this experiment. [1]

In pancreatic cancer–NK-cell cocultures, epacadostat at 100 nmol/L combined with PLP at 100 nmol/L increased tumor-cell death and NK-cell activation markers. The result supports this combination in the tested cocultures; it does not establish epacadostat monotherapy efficacy. [2]

Recombinant IDO1 and TDO inhibition

Biochemical assay · Recombinant human IDO1 and TDO, assayed separately [1]

Epacadostat inhibited rhIDO1 with a reported IC50 of 0.01 μM (SE = ±0.0009); the rhTDO IC50 was reported as >1 μM. These are assay endpoints under different substrate concentrations, not treatment doses or a universal selectivity ratio.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Inhibition of recombinant human IDO1-dependent kynurenine formationIC50 0.01 μM (SE = ±0.0009)[1]
Inhibition of recombinant human TDO-dependent kynurenine formationIC50 >1 μM[1]

Literature-Reported Treatment Conditions

Exposure duration
10-minute preincubation; 120-minute enzyme reaction at 37°C
Method
Concentration-response inhibition of kynurenine formation; Ehrlich reaction absorbance at 490 nm
Vehicle
2% DMSO
Reported limits
Exact tested epacadostat concentration series is not specified in the selected table. Salt/form and lot analytics are not specified.
Methods and source locations

Compound reported in the paper: Epacadostat (INCB024360); Compound label in the paper: epacadostat

Compound-level research evidence; no salt conversion, stereochemical equivalence or current Adooq lot validation inferred.

Table 1; Methods Enzyme assay (section7-11786469221138456)

Inhibition of recombinant human IDO1-dependent kynurenine formation: 0.3 μg/mL rhIDO1; 200 μM L-Trp. IC50 fits pooled 3 independent duplicate experiments. — Table 1; Methods Enzyme assay (section7-11786469221138456)

Inhibition of recombinant human TDO-dependent kynurenine formation: 0.8 μg/mL rhTDO; 2 mM L-Trp. IC50 fits pooled 3 independent duplicate experiments. — Table 1; Methods Enzyme assay (section7-11786469221138456)

Kynurenine inhibition in cells expressing IDO1 and TDO

Cell-based study · IFN-γ-stimulated human A172 glioblastoma cells [1]

Epacadostat decreased kynurenine production across the plotted 0.1–30 μM range without a comparable fall in the WST-8 viability signal. The dual inhibitor PVZB3001 suppressed kynurenine more strongly at ≥3 μM in this model. This experiment does not test epacadostat-mediated rescue of NK-cell killing.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Kynurenine production with a parallel cell-viability controlConcentration-response Kynurenine decreased; viability signal remained near control across the epacadostat series (qualitative)[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.1, 0.3, 1, 3, 10 and 30 μM
Exposure duration
1-hour pretreatment followed by 24 hours after L-Trp/IFN-γ addition
Method
Cell-based kynurenine assay and paired WST-8 viability readout
Vehicle
DMSO
Co-treatment
L-Trp 524 μM and IFN-γ 10 ng/mL; PVZB3001 and 680C91 tested separately as comparators
Reported limits
Final cellular DMSO percentage and exact salt/form are not specified in the selected methods.
Methods and source locations

Compound reported in the paper: Epacadostat (INCB024360); Compound label in the paper: epacadostat

Compound-level research evidence; no salt conversion, stereochemical equivalence or current Adooq lot validation inferred.

Figure 5A (epacadostat panel) and caption; Methods Cell-based Kyn production assay and Cell viability assay; Results section23

Kynurenine production with a parallel cell-viability control: Ehrlich reaction at 460 nm; WST-8 viability. Caption: representative of 3 independent experiments; means ± SD of triplicate samples; Dunnett comparison to control. — Figure 5A (epacadostat panel) and caption; Methods Cell-based Kyn production assay and Cell viability assay; Results section23

Epacadostat and PLP in pancreatic cancer–NK-cell coculture

Cell-based study · Human NK cells cocultured with T3M4 or CFPAC1 pancreatic cancer cells [2]

Combined epacadostat and pyridoxal 5′-phosphate (PLP) increased NK-associated tumor-cell death and the proportions of CD107a- and IFNγ-positive NK cells. Single-agent and NK-free controls were included. The increased killing is a combination effect in the coculture model.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Death of T3M4 and CFPAC1 cells with or without NK cellsTumor-cell death Combination increased tumor-cell death in NK cocultures (qualitative)[2]
CD107a-positive and IFNγ-positive NK-cell proportions in CFPAC1 cocultureNK activation markers Combination increased CD107a and IFNγ positivity (qualitative)[2]

Literature-Reported Treatment Conditions

Treatment concentration
Epacadostat 100 nmol/L; PLP 100 nmol/L
Method
Tumor-cell death and NK activation-marker measurements in coculture
Co-treatment
Epacadostat + PLP; each single agent and untreated control also evaluated
Reported limits
Duration for Figure 2A-C, explicit numerical n and final vehicle percentage could not be established from the read locations. S2 DMSO controls and its 72/96-hour 3D experiments are not transferred to Figure 2A-C.
Methods and source locations

Compound reported in the paper: Epacadostat (INCB024360); Compound label in the paper: IDO1i / INCB024360

Compound-level research evidence; no salt conversion, stereochemical equivalence or current Adooq lot validation inferred.

Figure 2A-C and caption; Results Targeting VB6 and Kynurenine pathways; Methods Cell Lines and Primary NK Cells and treatment/reagents

Death of T3M4 and CFPAC1 cells with or without NK cells: Figure 2A-B; mean ± SEM; two-way ANOVA with Tukey test. No bar heights converted to exact values. — Figure 2A-B and caption

CD107a-positive and IFNγ-positive NK-cell proportions in CFPAC1 coculture: Figure 2C; mean ± SEM; two-way ANOVA with Tukey test. — Figure 2C and caption

In Vivo Studies

In the orthotopic KPC1245 pancreatic tumor model, epacadostat plus PLP, with or without IL15, reduced tumor burden. Epacadostat, PLP and IL15 alone had tumor burdens comparable to control. [2]

In established AML xenografts, epacadostat-containing chow combined with Ara-C reduced bone-marrow and splenic AML burden. This small four-arm experiment used 1.6 g epacadostat/kg diet; that dietary concentration is not a body-weight-normalized daily dose. [3]

Antitumor activity was model-dependent. In the Eμ-TCL1 mouse CLL model, epacadostat at 4 mg/mouse daily by oral gavage did not provide sustained disease control, and endpoint spleen burden and leukemic-cell proliferation were similar to vehicle. [4]

Combination efficacy and single-agent limits in pancreatic tumors

Animal study · Syngeneic orthotopic KPC1245 pancreatic tumors in mice [2]

At the day-22 tumor-weight endpoint, epacadostat, PLP and IL15 monotherapies had tumor burdens comparable to control. Epacadostat plus PLP, with or without IL15, reduced tumor burden. Combination outcomes are not assigned to epacadostat monotherapy.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
KPC1245 tumor weight on day 22Tumor weight Single agents comparable to control; double/triple combinations reduced tumor weight (qualitative)[2]
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Saline control
No epacadostat		Reference groupReference tumor burden[2]
Epacadostat alone
100 mg/kg		Saline controlTumor burden comparable to control[2]
PLP alone
PLP 100 mg/kg		Saline controlTumor burden comparable to control[2]
Epacadostat + PLP
Epacadostat 100 mg/kg + PLP 100 mg/kg		Saline and corresponding single-agent groupsLower tumor weight than control; combination benefit[2]
IL15 alone
2 μg/mouse per administration		Saline controlTumor burden comparable to control[2]
Epacadostat + PLP + IL15
Epacadostat 100 mg/kg; PLP 100 mg/kg; IL15 2 μg/mouse per administration		Saline and single-agent groupsLower tumor weight than control[2]
Saline control
Model: Syngeneic orthotopic KPC1245 pancreatic tumors in mice
Treatment course: Tumor weight assessed on day 22
Vehicle: Saline
Epacadostat alone
Model: Syngeneic orthotopic KPC1245 pancreatic tumors in mice
Route: Oral gavage
Frequency: Daily
Treatment course: Started on day 7 after implantation; tumor-weight endpoint day 22
Reported limits: Drug formulation not specified in the read methods.
PLP alone
Model: Syngeneic orthotopic KPC1245 pancreatic tumors in mice
Route: Intraperitoneal
Frequency: Daily
Treatment course: Started on day 7 after implantation; tumor-weight endpoint day 22
Epacadostat + PLP
Model: Syngeneic orthotopic KPC1245 pancreatic tumors in mice
Route: Epacadostat: oral gavage; PLP: intraperitoneal
Frequency: Daily
Treatment course: Started on day 7 after implantation; tumor-weight endpoint day 22
IL15 alone
Model: Syngeneic orthotopic KPC1245 pancreatic tumors in mice
Route: Intraperitoneal
Frequency: Days 7, 9 and 11
Treatment course: Tumor-weight endpoint day 22
Epacadostat + PLP + IL15
Model: Syngeneic orthotopic KPC1245 pancreatic tumors in mice
Route: Epacadostat: oral gavage; PLP and IL15: intraperitoneal
Frequency: Epacadostat/PLP daily from day 7; IL15 days 7, 9 and 11
Treatment course: Tumor-weight endpoint day 22
Methods and source locations

Compound reported in the paper: Epacadostat (INCB024360); Compound label in the paper: IDO1i / INCB024360

Compound-level research evidence; no salt conversion, stereochemical equivalence or current Adooq lot validation inferred.

Figure 2D-E and caption; Supplementary Figure S2G (official PDF p.2); Methods Vitamin B6 Diet, Treatment, and Reagents

KPC1245 tumor weight on day 22: Mean ± SEM; one-way ANOVA with Tukey multiple comparisons. No exact tumor weights inferred from bars. — Figure 2E and caption; Figure 2D

Saline control · Figure 2D-E; Supplementary Figure S2G; Methods Vitamin B6 Diet, Treatment, and Reagents

Epacadostat alone · Figure 2D-E; Supplementary Figure S2G; Methods Vitamin B6 Diet, Treatment, and Reagents

PLP alone · Figure 2D-E; Supplementary Figure S2G; Methods Vitamin B6 Diet, Treatment, and Reagents

Epacadostat + PLP · Figure 2D-E; Supplementary Figure S2G; Methods Vitamin B6 Diet, Treatment, and Reagents

IL15 alone · Figure 2D-E; Supplementary Figure S2G; Methods Vitamin B6 Diet, Treatment, and Reagents

Epacadostat + PLP + IL15 · Figure 2D-E; Supplementary Figure S2G; Methods Vitamin B6 Diet, Treatment, and Reagents

Epacadostat chow and chemotherapy in established AML xenografts

Animal study · Established patient-derived AML xenografts in NSG mice [3]

A three-week four-arm experiment compared control chow, epacadostat chow, Ara-C and their combination. The combination reduced marrow and splenic AML burden. The authors described synergy only in marrow; this package reports the observed combination result without adopting a formal synergy claim.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
AML burden in bone marrow and spleen after combination treatmentAML burden Combination reduced marrow and spleen burden; control n = 4, Ara-C n = 3, epacadostat n = 4, combination n = 3[3]
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Control chow
No epacadostat or Ara-C		Reference groupReference AML burden; n = 4[3]
Epacadostat chow
1.6 g epacadostat/kg diet		Control chowAuthors report reduced marrow and spleen burden; n = 4[3]
Ara-C
60 mg/kg/day		Control chowModest marrow burden reduction at endpoint, described as not significant in Results; n = 3[3]
Epacadostat chow + Ara-C
Epacadostat 1.6 g/kg diet; Ara-C 60 mg/kg/day		Control chow and each single agentLower marrow and spleen AML burden; n = 3[3]
Control chow
Model: Established patient-derived AML xenografts in NSG mice
Frequency: Ad libitum chow
Treatment course: Three weeks; endpoint 11 weeks after transplant
Vehicle: Control chow
Epacadostat chow
Model: Established patient-derived AML xenografts in NSG mice
Route: Dietary
Frequency: Ad libitum
Treatment course: Three weeks from approximately week 8 after transplant
Vehicle: Supplemented chow
Reported limits: Diet concentration is not mg/kg body weight/day; intake not quantified.
Ara-C
Model: Established patient-derived AML xenografts in NSG mice
Route: Intraperitoneal
Frequency: Daily for 5 days
Treatment course: Days 1–5 of the three-week experiment
Vehicle: Control chow
Epacadostat chow + Ara-C
Model: Established patient-derived AML xenografts in NSG mice
Route: Epacadostat: dietary; Ara-C: intraperitoneal
Frequency: Chow ad libitum for 3 weeks; Ara-C daily for 5 days
Treatment course: Endpoint approximately 11 weeks after transplant
Vehicle: Supplemented chow
Reported limits: No body-weight dose inferred from diet concentration.
Methods and source locations

Compound reported in the paper: Epacadostat (INCB024360); Compound label in the paper: Epac. / epacadostat

Compound-level research evidence; no salt conversion, stereochemical equivalence or current Adooq lot validation inferred.

Figure 6I-K and caption; Methods Epacadostat; mouse models/combination therapy

AML burden in bone marrow and spleen after combination treatment: Mean ± SEM; Figure 6 caption specifies one-way ANOVA and additional unpaired t-test comparisons in marrow. Exact bar values are not reconstructed. — Figure 6J-K and caption; Results Pharmacologic targeting subsection

Control chow · Figure 6I-K and caption; Methods Epacadostat and Combination therapy

Epacadostat chow · Figure 6I-K and caption; Methods Epacadostat and Combination therapy

Ara-C · Figure 6I-K and caption; Methods Epacadostat and Combination therapy

Epacadostat chow + Ara-C · Figure 6I-K and caption; Methods Epacadostat and Combination therapy

Lack of sustained disease control in mouse CLL

Animal study · Syngeneic Eμ-TCL1 adoptive-transfer CLL model in wild-type mice [4]

Epacadostat produced a small, statistically nonsignificant early decrease in circulating CLL burden that disappeared later. Endpoint spleen weight, splenic tumor burden and CLL-cell KI67 positivity were similar to vehicle. The result limits generalization of antitumor activity across models.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Peripheral-blood CD5+CD19+ CLL-cell frequencyCLL progression Small nonsignificant early reduction; no sustained difference[4]
Spleen weight, splenic CLL burden and KI67-positive CLL cellsEndpoint disease burden No difference reported; endpoint control n = 6, epacadostat n = 7[4]

Conditions shared by the study groups

Route
Oral gavage
Frequency
Daily
Vehicle
0.5% methylcellulose
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Vehicle control
No epacadostat		Reference groupn = 8 allocated; n = 6 at endpoint[4]
Epacadostat
4 mg/mouse		Vehicle controlNo sustained CLL disease control; n = 8 allocated, n = 7 at endpoint[4]
Vehicle control
Model: Syngeneic Eμ-TCL1 adoptive-transfer CLL model in wild-type mice
Reported limits: Endpoint timing internally inconsistent; see review.
Epacadostat
Model: Syngeneic Eμ-TCL1 adoptive-transfer CLL model in wild-type mice
Treatment course: Started 2 weeks after transfer; exact endpoint duration unresolved
Reported limits: Figure 3 caption implies 3 treatment weeks; Results says 4 weeks. Do not convert dose to mg/kg.
Methods and source locations

Compound reported in the paper: Epacadostat (INCB024360); Compound label in the paper: Epa / INCB024360

Compound-level research evidence; no salt conversion, stereochemical equivalence or current Adooq lot validation inferred.

Figure 3A-D and caption; Results epacadostat paragraphs; Methods 2.5 and 2.6

Peripheral-blood CD5+CD19+ CLL-cell frequency: Means ± SEM; Welch t-test; blood plot labels weeks 0–3 after treatment start. — Figure 3A and Results epacadostat paragraph

Spleen weight, splenic CLL burden and KI67-positive CLL cells: Means ± SEM; Welch t-test. Four of 20 mice excluded before allocation for failed engraftment; 8/group treated, with 2 control and 1 treated deaths before endpoint analysis. — Figure 3B-D and caption; Methods 2.5

Vehicle control · Figure 3A-D and caption; Methods 2.5; Results epacadostat paragraphs

Epacadostat · Figure 3A-D and caption; Methods 2.5; Results epacadostat paragraphs

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 1204669-58-8
Alternate CAS 1204669-37-3
Applications IDO inhibitor
Formula C11H13BrFN7O4S
Molecular Weight 438.23
Synonyms INCB 024360
SMILES
C1=CC(=C(C=C1NC(=C2C(=NON2)NCCNS(=O)(=O)N)N=O)Br)F

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 74 mg/mL (168.86 mM)
Water Insoluble
Ethanol Warmed: 45 mg/mL

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
4.13 mg/mL
Vehicle
5% DMSO+40% PEG 300+5% TWEEN 80+50 % ddH2O

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Saeko Yoshioka, Tomonori Ikeda, Sogo Fukuchi, et al. Identification and Characterization of a Novel Dual Inhibitor of Indoleamine 2,3-dioxygenase 1 and Tryptophan 2,3-dioxygenase International journal of tryptophan research : IJTR (2022). PMID: 36467776 DOI: 10.1177/11786469221138456 Source material
  2. [2] Chunbo He, Dezhen Wang, Surendra K Shukla, et al. Vitamin B6 Competition in the Tumor Microenvironment Hampers Antitumor Functions of NK Cells Cancer discovery (2024). PMID: 37931287 DOI: 10.1158/2159-8290.cd-23-0334 Source material
  3. [3] Marta Galán-Díez, Florence Borot, Abdullah Mahmood Ali, et al. Subversion of Serotonin Receptor Signaling in Osteoblasts by Kynurenine Drives Acute Myeloid Leukemia Cancer discovery (2022). PMID: 35046097 DOI: 10.1158/2159-8290.cd-21-0692 Source material
  4. [4] Selcen Öztürk, Verena Kalter, Philipp M. Roessner, et al. IDO1-Targeted Therapy Does Not Control Disease Development in the Eµ-TCL1 Mouse Model of Chronic Lymphocytic Leukemia Cancers (2021). PMID: 33920868 DOI: 10.3390/cancers13081899 Source material

Publications

3 publications citing this product

  1. Chunbo He, .et al. , Cancer Discov, 2024, Jan 12;14(1):176-193 PMID: 37931287
  2. Saeko Yoshioka, .et al. , Int J Tryptophan Res, 2022, Nov 30;15 PMID: 36467776
  3. Marta Galan-Diez, .et al. , Cancer Discov, 2022, Apr 1;12(4):1106-1127 PMID: 35046097

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