p70S6K

4EBP1

mTORC1

Ras-MAPK PLCγ-PKC STAT

STAT

MYC

STATSTAT

JAKJAK

AKT

PIM

PIMpim

c-myc

PI3Kδ

B-Cell ReceptorCytokine/Growth Factor Receptor FGF Receptor

BAD

Growth/Survival

Proliferation

Survival

BET

TARGETEDTHERAPIESOverview of Clinical Trials

NFκB

Science Drives SuccessIncyte is a company founded on the premise that investment in good science and the rigorous pursuit of R&D excellence can translate into new medicines that can positively affect patients’ lives.

Our pipeline includes a number of targeted therapies at various stages of clinical development.

Our strategy relies on intervention at critical components of interdependent signaling pathways, acting at the following levels:

Extracellular receptors:receptor tyrosine kinases that initiate intracellular signaling pathways involved in cellular proliferation, migration, and survival

Intracellular protein and lipid kinases:primary effectors that transduce signaling of key pathways (eg, JAK-STAT, PI3K/AKT)

Epigenetic regulators:downstream effectors of signaling pathways that regulate gene expression via histone modification

The rigorous pursuit of scientific excellence remains at the core

of our company today

The efficacy and safety of the investigational compounds discussed in this brochure have not been established. There is no guarantee that these compounds will become commercially available for the use(s) under investigation.

Recruiting and Upcoming Trials

TRIAL TREATMENT ARM(S) PHASE CCA CRS GVHD UCHEME

TUMORSSOLID

TUMORS PAGE

Itacitinib (INCB039110)

Itacitinib + CS or placebo + CS 3 CHRONIC 7

Itacitinib + calcineurin inhibitor–based interventions 1 PROPHYLAXIS 8

INCB 39110-211 Itacitinib + immune effector cell therapy 2 ● 9

Ponatinib (INCB084344)

INCB 84344-102 Ponatinib monotherapy 1/2 ● ● 11

Tafasitamab (MOR208)Tafasitamab + bendamustine vs rituximab + bendamustine 2/3 R/R DLBCL 13

Tafasitamab + R-CHOP ± lenalidomide 1b DLBCL 13

Pemigatinib (INCB054828)

Pemigatinib monotherapy vs gemcitabine + cisplatin 3 ● 15

Pemigatinib + pembrolizumab vs pemigatinib vs SOC 2 ● 15

Pemigatinib monotherapy 2 8p11 MLN 16

Pemigatinib monotherapy 2 ● 16

Pemigatinib monotherapy and combination therapy 1/2 ● ● ● ● 17

POD1UM-204 Retifanlimab (PD-1 inhibitor) monotherapy + pemigatinib or epacadostat (IDO1 inhibitor) 2 ● 17

3

Recruiting and Upcoming Trials (cont)

TRIAL TREATMENT ARM(S) PHASE CCA CRS GVHD UCHEME

TUMORSSOLID

TUMORS PAGE

Parsaclisib (INCB050465)

Parsaclisib monotherapy 2 FL 19

Parsaclisib + investigator choice of rituximab, bendamustine + rituximab, or ibrutinib 1 NHL 20

INCB 50465-201 Parsaclisib + ruxolitinib 2 MF 21

POD1UM-102 Retifanlimab (PD-1 inhibitor) + epacadostat (IDO1 inhibitor) or parsaclisib 1b ● 21

4

Recruiting and Upcoming Trials (cont)

TRIAL TREATMENT ARM(S) PHASE CCA CRS GVHD UCHEME

TUMORSSOLID

TUMORS PAGE

BET Inhibitor (INCB057643)

INCB 57643-103 INCB057643 monotherapy 1 MF 23

ALK2 inhibitor (INCB000928)

INCB 000928-104 INCB000928 monotherapy or combined with ruxolitinib 1/2 MPD 25

5

JAK JANUS KINASE

STAT

STAT

MYC

PIM

STAT

JAK

pim

c-myc

PIM

p70S6K

4EBP1

BAD

Survival

mTORC1

Growth/Survival

Cytokine/Growth Factor Receptor

Incyte is developing an inhibitor of JAK• Itacitinib (INCB039110)

− Investigational, orally bioavailable, selective inhibitor of JAK1: 22-fold higher selectivity for JAK1 over JAK29

− Mean IC50 (enzyme assays) for JAK1 and JAK2: 3.6 and 80 nM, respectively9

JAK: JANUS KINASE• The JAK family of nonreceptor tyrosine

kinases JAK1, JAK2, JAK3, and TYK2 associates with a wide variety of cytokine and growth factor receptors1

• On receptor activation, JAK dimers promote phosphorylation of transcription factors (STATs) that regulate the downstream transcription of several target genes1-3

• Aberrant activation of the JAK-STAT pathway has been associated with hematopoietic malignancies, such as myeloproliferative neoplasms (MPNs), including myelofibrosis (MF), polycythemia vera (PV), and essential thrombocythemia (ET)4

• In solid tumors, signals transduced via JAK may promote a variety of biological processes considered to be hallmarks or enabling characteristics of cancer5-8

1. Jatiani SS, et al. Genes Cancer. 2011;1:979-993. 2. Kiu H, Nicholson SE. Growth Factors. 2012;30:88-106. 3. Yu H, et al. Nat Rev Cancer. 2009;9:798-809. 4. Rampal R, et al. Blood. 2014;123:e123-e133. 5. Thoennissen NH, et al. Cancer Res. 2009;69:5876-5884. 6. Toyonaga T, et al. Cancer Lett. 2003;201:107-116. 7. Iwanski GB, et al. Br J Pharmacol. 2010;160:998-1007. 8. Koblish HK, et al. Cancer Res. 2015;75(15 suppl). AACR 2015. Poster 1336. 9. Data on file. Incyte Corporation. 6

JAKJANUS KINASE

GRAVITAS: GRAft-Versus-Host Disease Outcomes Evaluation via JAK1 Inhibitor ITAcitinib Clinical Studies

Steroid-Naive Chronic GVHD

A Randomized, Double-Blind, Phase 3 Study of Itacitinib or Placebo in Combination With Corticosteroids as First-Line Treatment

• Primary outcome measures:− Part 1: number of dose-limiting toxicities through day 28− Part 2: response rate at month 6

• Study population: patients with active, clinically diagnosed, moderate or severe cGVHD per NIH consensus criteria− Patients who underwent alloHSCT from any donor HLA type using any graft source

− Patients must not have received > 72 hours of systemic corticosteroid treatment for cGVHD or JAK inhibitor therapy for acute GVHD (unless the participant achieved a complete or partial response and has been off JAK inhibitor treatment for ≥ 8 weeks before randomization)

NCT03584516

7

JAK JANUS KINASE

GRAVITAS: GRAft-Versus-Host Disease Outcomes Evaluation via JAK1 Inhibitor ITAcitinib Clinical Studies

Prophylaxis of GVHD

An Open-Label, Single-Arm, Phase 1 Study of Itacitinib in Combination With Calcineurin Inhibitor–Based Interventions

• Primary outcome measure: proportion of patients with hematologic recovery (neutrophil and platelet counts) at day 28

• Study population:

− Patients must be candidates for peripheral blood stem cell transplants and reduced-intensity conditioning regimens

− The CNI-based prophylaxis regimen will be identified by the investigator before the patient’s enrollment and will consist of the combination of Tac + MTX or CsA + MMF. ATG may be included at the treating investigator’s discretion

NCT03320642

8

JAKJANUS KINASE

JAK1 Inhibitor: Itacitinib (INCB039110)

Cytokine Release Syndrome

A Single-Arm, Open-Label, Phase 2 Study of Itacitinib for the Prevention of Cytokine Release Syndrome Induced by Immune Effector Cell Therapy

• Primary outcome measure: proportion of patients who develop grade ≥ 2 CRS

• Study population: patients aged ≥ 12 years who are planning to receive Kymriah (tisagenlecleucel) or Yescarta (axicabtagene ciloleucel) IEC therapy for any approved hematologic indication

NCT04071366

INCB 39110-211

9

BCR-ABL1 BREAKPOINT CLUSTER REGION-ABELSON TYROSINE KINASE

JAK2/STATMAPK/ERK

AKT TRAIL

Apoptosis

mTOR

Uncontrolled Cell Proliferation

Genomic Instability

CCAAT/EBP

BCR-ABL1

1. Ronson A, et al. Curr Treat Options Oncol. 2017;18:20. 2. Lee HJ, et al. Cancer. 2011;117:1583-1594. 3. Pane F, et al. Oncogene. 2002;21:8652-8667. 4. Kang ZJ, et al. Chin J Cancer. 2016;35:48. 5. Iclusig (ponatinib) [summary of product characteristics]. 2019. 6. Tan FH, et al. Onco Targets Ther. 2019;12:635-645.

Ponatinib: tyrosine kinase inhibitor• Iclusig® (ponatinib) is indicated in the European Union for treatment of adult patients with5:

− Chronic phase, accelerated phase, or blast phase CML who are resistant to dasatinib or nilotinib, who are intolerant of dasatinib or nilotinib and for whom subsequent treatment with imatinib is not clinically appropriate, or who have the T315I mutation

− Philadelphia chromosome–positive ALL who are resistant to dasatinib who are intolerant of dasatinib and for whom subsequent treatment with imatinib is not clinically appropriate, or who have the T315I kinase domain mutation

• Iclusig® (ponatinib) showed efficacy against other tyrosine kinases (eg, c-KIT, c-SRC, FGFR, FLT3, PDGFR, RET, and VEGFR)5,6

BCR-ABL1: BREAKPOINT CLUSTER REGION-ABELSON TYROSINE KINASE• The BCR-ABL1 oncogene is expressed

on the Philadelphia chromosome1

• The Philadelphia chromosome is generated by the reciprocal translocation of the ABL1 gene, located on chromosome 9, to BCR, located on chromosome 22, resulting in the BCR-ABL1 oncogene1

• BCR-ABL1 fusion proteins are constitutively active tyrosine kinases that alter multiple signaling pathways, contributing to the growth and proliferation of B lineage cells2-4

PI3Kδ

Microenvironment for Leukemia

Stem Cells

Inhibition of Cell Differentiation

Uncontrolled Cell Proliferation

Cell Survival

10

BCR-ABL1BREAKPOINT CLUSTER REGION-ABELSON TYROSINE KINASE

Tyrosine Kinase Inhibitor: Ponatinib (INCB084344)

Relapsed or Refractory Leukemias, Lymphomas, or Solid Tumors

An Open-Label, Single-Arm, Phase 1/2 Study of Ponatinib in Pediatric Patients, With an Expansion Group in Pediatric Patients With CP-CML

• Primary outcome measures:− Phase 1: number of dose-limiting toxicities− Phase 2: efficacy

• Study population: patients with histologically or cytologically confirmed diagnosis of any of the following malignancies: CP-CML, BP-CML, AP-CML; ALL; AML; other leukemias; lymphoma; any other tumors, including tumors of the CNS, for which standard therapy is not available or is not indicated− In phase 1, patients with CP-CML are required to be resistant to or intolerant of ≥ 1 prior BCR-ABL–targeted TKI therapy;

in phase 2, they are required to be resistant to or intolerant of ≥ 1 prior BCR-ABL–targeted TKI therapy or have the T315l kinase domain mutation

− Patients aged ≥ 1 to < 18 years

NCT03934372

INCB 84344-102

11

CD19 CLUSTER OF DIFFERENTIATION 19

BCR

SYK

PIP

CD19

PI3K

BTK

B-cell receptor signaling

Survival Proliferation

Differentiation

PIP

1. Del Nagro CJ, et al. Immunol Res. 2005;31:119-131. 2. Blanc V, et al. Clin Cancer Res. 2011;17:6448-6458. 3. Katz B, Herishanu Y. Leuk Lymphoma. 2014;55:999-1006. 4. Poe JC, et al. J Immunol. 2012;189:2318-2325. 5. Monjuvi (tafasitamab-cxix) [prescribing information]. 2020. 6. Incyte Corporation [press release]. https://investor.incyte.com/news-releases/news-release-details/morphosys-and-incyte-sign-global-collaboration-and-license. Accessed May 5, 2020.

Tafasitamab: CD19-directed antibody• Tafasitamab is indicated in the United States in combination with lenalidomide for the treatment

of adults with relapsed or refractory DLBCL not otherwise specified, including DLBCL arising from low grade lymphoma, and who are not eligible for autologous HSCT5

• Incyte has entered into a collaboration and license agreement with MorphoSys to develop and commercialize tafasitamab (MOR208), an Fc-engineered anti-CD19 antibody6

CD19: CLUSTER OF DIFFERENTIATION 19• The human CD19 antigen is a 95-kD

transmembrane glycoprotein belonging to the immunoglobulin superfamily1

• CD19 is expressed from the early pre-B stage throughout B-cell differentiation up to mature B cells before downmodulation at the plasma cell stage. It plays a key role in B-cell differentiation, proliferation, and signaling 2,3

• CD19 expression is maintained across different B cell-derived blood cancers2

• CD19 enhances BCR signaling and tumor cell proliferation4

12

CD19CLUSTER OF DIFFERENTIATION 19

CD19-directed antibody: Tafasitamab (MOR208)

Relapsed or Refractory Diffuse Large B-Cell Lymphoma

A Phase 2/3, Randomized, Multicenter Study of Tafasitamab vs Rituximab Both in Combination With Bendamustine

• Primary outcome measure: progression-free survival• Study population: patients with histologically confirmed diagnosis per WHO 2008 criteria of DLBCL NOS, THRLBCL, EBV-positive

DLBCL, composite lymphoma with a DLBCL component (with a DLBCL relapse after DLBCL treatment), or disease transformed from an earlier diagnosis of low-grade lymphoma to DLBCL (with a DLBCL relapse after DLBCL treatment); patients must be ineligible for high-dose chemotherapy and autologous stem cell transplant

B-MIND is a MorphoSys-sponsored, randomized, two-arm, multicenter, open-label, phase 2/3 trial co-funded with Incyte to evaluate the efficacy and safety of tafasitamab with bendamustine versus rituximab with bendamustine in adult patients with relapsed or refractory DLBCL. Tafasitamab is an investigational, humanized, Fc-engineered monoclonal antibody directed against CD19, in-licensed by Incyte from MorphoSys and jointly developed by Incyte and MorphoSys since 2020, when the parties entered into a collaboration and license agreement. MorphoSys and Incyte will co-commercialize tafasitamab in the U.S., while Incyte has exclusive commercialization rights outside of the U.S. NCT02763319

Diffuse Large B-Cell Lymphoma

A Phase 1b, Open-Label, Randomized Study of Tafasitamab in Combination With R-CHOP With or Without Lenalidomide

• Primary outcome measure: treatment-emergent adverse events

• Study population: patients with histologically confirmed, newly diagnosed DLBCL NOS that was previously untreated

First-MIND is a MorphoSys-sponsored, randomized, multicenter, open-label, phase 1b trial co-funded with Incyte to evaluate the safety and preliminary efficacy of tafasitamab in addition to R-CHOP, or tafasitamab and lenalidomide in addition to R-CHOP, in adult patients with newly diagnosed, previously untreated DLBCL. Tafasitamab is an investigational, humanized, Fc-engineered monoclonal antibody directed against CD19, in-licensed by Incyte from MorphoSys and jointly developed by Incyte and MorphoSys since 2020 when the parties entered into a collaboration and license agreement. MorphoSys and Incyte will co-commercialize tafasitamab in the U.S., while Incyte has exclusive commercialization rights outside of the U.S. NCT04134936

13

FGFR FIBROBLAST GROWTH FACTOR RECEPTOR

AKT

STAT

FGFR RAS

MAPK

RAF

MEK

p70S6K

4EBP1

BADSurvival

mTORC1

Growth/SurvivalCell Cycle Genes

PI3K

Proliferation

Pemigatinib: FGFR1/2/3 inhibitor• Pemazyre® (pemigatinib) is indicated in the United States for the treatment of adults with

previously treated, unresectable, locally advanced or metastatic cholangiocarcinoma with a FGFR2 fusion or other rearrangement as detected by an FDA-approved test12

• Pemazyre® (pemigatinib)− Investigational, orally bioavailable, selective inhibitor of FGFR1, FGFR2, and FGFR313

− Mean IC50 (enzyme assays) for FGFR1, FGFR2, FGFR3, and FGFR4: 0.4, 0.5, 1, and 30 nM, respectively13

FGFR: FIBROBLAST GROWTH FACTOR RECEPTOR• The FGFR family includes 4

membrane-associated receptor kinases, known as FGFR1-41,2

• After ligand binding, FGFRs dimerize and activate downstream signaling pathways involved in regulating cellular proliferation, survival, and migration2-4

• Activating mutations, translocations, and gene amplifications in FGFRs have been implicated in tumor cell proliferation, angiogenesis, metastasis, and survival2

• Examples include:− FGFR1 gene amplification in

squamous cell lung cancer5

− Chromosomal translocation involving FGFR1 in 8p11 myeloproliferative syndrome6

− FGFR2 gene amplification in gastric cancer7 and FGFR2 translocation in intrahepatic CCA8,9

− FGFR3-activating mutations and translocations in bladder cancer10,11

1. Turner N, Grose R. Nat Rev Cancer. 2010;10:116-129. 2. Liang G, et al. Trends Pharmacol Sci. 2012;33:531-541. 3. Belov AA, Mohammadi M. Cold Spring Harb Perspect Biol. 2013;5:a015958. 4. Teven CM, et al. Genes Dis. 2014;1:199-213. 5. Weiss J, et al. Sci Transl Med. 2010;2:62ra93. 6. Hallinan N, et al. Cancer Treat Rev. 2016;46:51-62. 7. Matsumoto K, et al. Br J Cancer. 2012;106:727-732. 8. Arai Y, et al. Hepatology. 2014;59:1427-1434. 9. Ang C. J Gastroenterol Hepatol. 2015;30:1116-1122. 10. Gust KM, et al. Mol Cancer Ther. 2013;12:1245-1254. 11. Williams SV, et al. Hum Mol Genet. 2013;22:795-803. 12. Pemazyre (pemigatinib) [prescribing information]. 2020. 13. Liu PCC, et al. PLoS One. 2020;15(4):e0231877. 14

FGFRFIBROBLAST GROWTH FACTOR RECEPTOR

FIGHT: FIbroblast Growth Factor Receptor Inhibitor in Oncology and Hematology Trials

Cholangiocarcinoma

A Randomized, Open-Label, Phase 3 Study of Pemigatinib vs Gemcitabine Plus Cisplatin in First-Line Treatment

• Primary outcome measure: progression-free survival

• Study population: patients with unresectable or metastatic CCA with documented FGFR2 rearrangement

− Patients must not have received prior anticancer systemic therapy

NCT03656536

Urothelial Carcinoma

A Randomized, Open-Label, Phase 2 Study of Pemigatinib Plus Pembrolizumab vs Pemigatinib Alone vs Standard of Care in First-Line Treatment

• Primary outcome measure: progression-free survival

• Study population: patients with metastatic or unresectable urothelial carcinoma and documented FGFR3 mutation or rearrangement

− Patients must be ineligible to receive cisplatin. Patients ineligible for any platinum-based chemotherapy are allowed

− Patients must not have received prior systemic therapy for metastatic or unresectable disease (except adjuvant or neoadjuvant platinum-based chemotherapy with recurrence > 12 months since completion of therapy)

NCT04003610

15

FGFR FIBROBLAST GROWTH FACTOR RECEPTOR

FIGHT: FIbroblast Growth Factor Receptor Inhibitor in Oncology and Hematology Trials

8p11 Myeloid/Lymphoid Neoplasm

An Open-Label, Phase 2 Study to Evaluate the Efficacy and Safety of Pemigatinib• Primary outcome measure: proportion of patients who achieve CR based on response criteria for myeloid or lymphoid

neoplasms with FGFR1 rearrangement

• Study population: patients with documented myeloid or lymphoid neoplasm with 8p11 rearrangement known to lead to FGFR1 activation, based on cytogenetic evaluation− Patients must have relapsed after HSCT or other disease-modifying therapy or not be current candidates for HSCT

or other disease-modifying therapies− All patients with relapsed or refractory disease must have evidence of either cytogenetic or hematologic disease and

have no evidence of residual toxicity (eg, GVHD requiring treatment)NCT03011372

Solid Tumors With FGFR1/2/3 Alterations

An Open-Label, Phase 2 Study to Evaluate the Efficacy and Safety of Pemigatinib

• Primary outcome measure: objective response rate

• Study population: patients with advanced or metastatic or surgically unresectable solid tumor malignancies− Patients must have documented FGFR1-3 mutations or translocations, have experienced objective progression

with ≥ 1 prior therapy, and have no therapy available that is likely to provide clinical benefit

NCT03822117

16

FGFRFIBROBLAST GROWTH FACTOR RECEPTOR

FIGHT: FIbroblast Growth Factor Receptor Inhibitor in Oncology and Hematology Trials

Solid and Hematologic Tumors

An Phase 1/2, Open-Label, 3-Part Study of Pemigatinib• Primary outcome measures: maximum tolerated dose of pemigatinib as monotherapy and in combination with

other agents (gemcitabine + cisplatin, pembrolizumab, docetaxel, trastuzumab, or retifanlimab [PD-1 inhibitor]; pharmacodynamics of pemigatinib as measured by serum phosphorus levels

• Study population:− Part 1 (dose escalation): patients with any advanced solid tumor malignancy− Part 2 (dose expansion): patients with squamous NSCLC, CCA/gastric cancer, urothelial cancer, breast/endometrial

cancer, MM, or MPNs who have a tumor or malignancy harboring FGF/FGFR alterations− Part 3 (combination therapy), dose finding: patients with solid tumor malignancies; dose expansion:

FGF/FGFR+ patients NCT02393248

Endometrial Cancer

A Nonrandomized, Open-Label, Umbrella, Phase 2 Study of Retifanlimab (PD-1 inhibitor) Alone or Combined With Pemigatinib or Epacadostat (IDO1 Inhibitor)

• Primary outcome measures: objective response rate (in MSI-high group receiving retifanlimab monotherapy)

• Study population: patients with advanced or metastatic endometrial cancer that has progressed on or after ≥ 1 platinum-containing regimen

NCT04463771

17

PI3Kδ PHOSPHATIDYLINOSITOL 3-KINASE DELTA

AKTPI3Kδ

p70S6K

4EBP1

BAD

Survival

mTORC1

Growth/Survival

BCR

Incyte is developing an inhibitor of PI3Kδ signaling: parsaclisib

• Parsaclisib (INCB050465) is an investigational, orally bioavailable, and selective PI3Kδ inhibitor6

• In enzyme assays, parsaclisib inhibited PI3Kδ (IC50 = 1 nM), with approximately 20,000-fold selectivity for PI3Kα, -β, and -γ6

PI3Kδ: PHOSPHATIDYLINOSITOL 3-KINASE DELTA• PI3Ks are heterodimeric lipid kinases

activated by several receptor types, including B-cell receptors1

• There are 4 isoforms of class I PI3K catalytic subunits: p110α, -β, -γ, and -δ1

• The PI3Kδ isoform is preferentially expressed in hematopoietic cells1

• PI3Kδ activation initiates numerous downstream effects on cell survival and growth, protein synthesis, and inhibition of apoptosis1,2

• Constitutive activation of B-cell receptors and signaling via the PI3Kδ pathway drives B-cell malignancies, including NHL and HL1-4

• Emerging data suggest that PI3Kδmay also be an important target in solid tumors5

1. Puri K, Gold MR. Front Immunol. 2012;3:256. 2. Ortiz-Maldonado V, et al. Ther Adv Hematol. 2015;6:25-36. 3. Akinleye A, et al. J Hematol Oncol. 2013;6:88. 4. Castillo J, et al. Onco Targets Ther. 2014;7:333-342. 5. Ali K, et al. Nature. 2014;510:407-411. 6. Forero-Torres A, et al. Blood. 2019;133:1742-1752. 18

PI3KδPHOSPHATIDYLINOSITOL 3-KINASE DELTA

CITADEL: Clinical Investigation of TArgeted PI3K-DELta Inhibition in Lymphomas

Relapsed or Refractory Follicular Lymphoma

An Open-Label, Phase 2 Study of Parsaclisib

• Primary outcome measure: objective response rate

• Study population: patients with histologically confirmed, relapsed or refractory, follicular B-cell NHL (FL) grade 1, 2, or 3a; must be ineligible for HSCT

− Patients must have no known histological transformation from indolent NHL to DLBCL and have not received prior treatment with PI3Kδ, pan-PI3K, or BTK inhibitors

NCT03126019

19

PI3Kδ PHOSPHATIDYLINOSITOL 3-KINASE DELTA

CITADEL: Clinical Investigation of TArgeted PI3K-DELta Inhibition in Lymphomas

Relapsed or Refractory B-Cell Lymphoma

An Open-Label, Dose-Finding, Phase 1 Study of Parsaclisib in Combination With Investigator Choice of Rituximab, Bendamustine + Rituximab, or Ibrutinib

• Primary outcome measure: safety and tolerability

• Study population: patients with histologically confirmed indolent/aggressive DLBCL, FL, MZL, or MCL

NCT03424122

20

PI3KδPHOSPHATIDYLINOSITOL 3-KINASE DELTA

PI3Kδ Inhibitor: Parsaclisib (INCB050465)

Myelofibrosis

An Open-Label, Phase 2, 4-Part Study of Parsaclisib in Combination With Ruxolitinib

• Primary outcome measures:− Part 1: number of patients with dose-limiting toxicities− Parts 2, 3, and 4: change from baseline in spleen volume at week 12 as measured by MRI or CT scan

• Study population: patients with primary MF, post-PV MF, or post-ET MF on existing stable regimen of ruxolitinib− Patients must have palpable spleen of > 10 cm or palpable splenomegaly of 5 to 10 cm and active symptoms at the

screening visit

NCT02718300

INCB 50465-201

Solid Tumors

An Open-Label, Dose-Escalation, Phase 1b Study of Retifanlimab (PD-1 inhibitor) in Combination With Epacadostat (IDO1 Inhibitor) or Parsaclisib

• Primary outcome measures: safety, determination of RP2D for each combination

• Study population: patients with histologically proven, locally advanced, unresectable or metastatic solid tumors for whom no approved therapy with demonstrated clinical benefit is available or who are intolerant of or have declined standard therapy

NCT03589651

21

BET BROMODOMAIN (BRD) AND EXTRATERMINAL DOMAIN PROTEIN

BET

NFκB Inflammatory Signaling

1. Belkina AC, et al. Nat Rev Cancer. 2012;12(7):465-477. 2. Delmore JE, et al. Cell. 2011;146(6):904-917. 3. Huang B, et al. Mol Cell Biol. 2009;29(5):1375-1387. 4. Kleppe M, et al. Cancer Cell. 2018;33:29-43.e7. 5. Data on file. Incyte Corporation.

Incyte is developing an inhibitor of BET proteins• Incyte is developing an inhibitor of BET5

• INCB057643 was shown to prevent BET proteins from interacting with acetylated histones to inhibit pro-inflammatory gene expression5

BET: BROMODOMAIN AND EXTRATERMINAL DOMAIN PROTEINS• The BET family of proteins are

epigenetic readers that regulate transcription of genes involved in cell growth, survival, and inflammation through the formation of chromatin-modifying transcriptional complexes1,2

• Members of the BET family have been shown to regulate the activity of NFκB, a cancer-associated transcription factor, and other pro-inflammatory gene programs that contribute to chronic inflammatory diseases such as myeloproliferative neoplasms3,4

• In a mouse model of myelofibrosis, BET inhibition reduced NFκB-driven inflammatory signaling and in turn reduced bone marrow fibrosis and improved survival4

22

BETBROMODOMAIN (BRD) AND EXTRATERMINAL DOMAIN PROTEIN

BET Inhibitor: INCB057643

Myelofibrosis

An Open-Label, Phase 1 Study of INCB057643

• Primary outcome measure: safety and tolerability

• Study population: patients with relapsed or refractory primary MF or secondary MF (post-PV MF, post-ET MF)− Patients must not be candidates for potentially curative therapy, including HSCT

NCT04279847

INCB 57643-103

23

ALK2 ACTIVIN RECEPTOR-LIKE KINASE 2

SMAD1/5/8

BMPRII

BMP

Hepcidin

Hepatocyte

ALK2

SMAD4

hamp

1. Ganz T. Blood. 2011;117:4425-4433. 2. Birgegard G, et al. Eur J Haematol. 2019;102:235-240. 3. Steinbicker AU, et al. Blood. 2011;118:4224-4230. 4. Asshoff M, et al. Blood. 2017;129:1823-1830. 5. Data on file. Incyte Corporation.

Incyte is developing an inhibitor of ALK2• INCB000928 is an potent, selective, small-molecule inhibitor of ALK25

• INCB000928 decreased hepcidin levels and improved anemia in a preclinical model5

ALK2: ACTIVIN RECEPTOR-LIKE KINASE 2• States of heightened inflammation

with anemia exist in several diseases, including hematologic malignancies such as myelofibrosis and some solid tumors1,2

• Elevated levels of cytokines in these conditions stimulate increases in serum concentrations of hepcidin, which—through its degradation of ferroportin—leads to a functional iron deficiency1

• Cytokine-induced hepcidin gene transcription can be activated through the BMP signaling pathway, which is regulated by the type I BMP receptor ALK23

• In patients with myelofibrosis who are transfusion-dependent or present with symptomatic anemia, ALK2 inhibition may reduce hepcidin levels and improve anemia4

24

ALK2ACTIVIN RECEPTOR-LIKE KINASE 2

ALK2 inhibitor: INCB000928

Myeloproliferative Disorders

An phase 1/2 open-label, dose-finding, 2-part study of INCB000928 as monotherapy or in combination with ruxolitinib

• Primary outcome measures: safety and tolerability

• Study population: patients with myelofibrosis who are transfusion-dependent or present with symptomatic anemia

NCT04455841

INCB 00928-104

25

Abbreviations• AE = adverse event

• ALK = activin receptor-like kinase

• alloHSCT = allogeneic hematopoietic stem cell transplant

• ATG = antithymocyte globulin

• BET = bromodomain and extraterminal domain

• BMP = bone morphogenetic protein

• BRD = bromodomain-containing protein

• BTK = Bruton’s tyrosine kinase

• CCA = cholangiocarcinoma

• cGVHD = chronic graft-vs-host disease

• CITADEL = Clinical Investigation of Targeted PI3K-Delta Inhibition in Lymphomas

• CR = complete response

• CRS = cytokine release syndrome

• CS = corticosteroids

• CsA + MMF = cyclosporine + mycophenolate mofetil

• CT = computed tomography

• DLBCL = diffuse large B-cell lymphoma

• EBV = Epstein-Barr virus

• ET = essential thrombocythemia

• FGF = fibroblast growth factor

• FIGHT = Fibroblast Growth Factor Receptor Inhibitor in Oncology and Hematology Trials

• FL = follicular lymphoma

• GRAVITAS = Graft-Versus-Host Disease Outcomes Evaluation via JAK1 Inhibitor Itacitinib Clinical Studies

• GVHD = graft-vs-host disease

• HCC = hepatocellular carcinoma

• HL = Hodgkin lymphoma

• HLA = human leukocyte antigen

• HSCT = hematopoietic stem cell transplant

• IC50 = half maximal inhibitory concentration

• I-DAC = intermediate-dose cytarabine

• IEC = immune effector cell

• JAK = Janus kinase

• MAO-A = monoamine oxidase A

• MAO-B = monoamine oxidase B

• MCL = mantle cell lymphoma

• MF = myelofibrosis

• MLN = myeloid lymphoid neoplasm

• MM = multiple myeloma

• MPD = myeloproliferative disorders

• MPN = myeloproliferative neoplasm

• MRI = magnetic resonance imaging

• MZL = marginal zone lymphoma

• NHL = non-Hodgkin lymphoma

• NOS = not otherwise specified

• NSCLC = non-small cell lung cancer

• PD-1 = programmed cell death 1 protein

• PI3K = phosphatidylinositol 3-kinase

• PV = polycythemia vera

• R-CHOP = rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone

• R/R = relapsed or refractory

• SOC = standard of care

• STAT = signal transducer and activator of transcription

• Tac + MTX = tacrolimus + methotrexate

• THRLBCL = T-cell/histiocyte-rich large B-cell lymphoma

• TYK2 = tyrosine kinase 2

• UC = urothelial carcinoma

To learn more about these ongoing clinical studies or to learn about becoming a study site:

Contact us at clintrials@incyte.com

For any general medical information requests:

Outside the US: Contact us at globalmedinfo@incyte.com

For US: Contact us at 1-855-4MEDINFO (1-855-463-3463) or by email at medinfo@incyte.com

The efficacy and safety of the investigational compounds discussed in this brochure have not been established. There is no guarantee that these compounds will become commercially available for the use(s) under investigation.

For more information, visit: www.incyte.comFOLLOW INCYTE ON SOCIAL MEDIATwitter: http://twitter.com/incyteLinkedIn: https://linkedin.com/company/incyte

The information in this brochure is current as of July 28, 2020.© 2020, Incyte Biosciences International Sàrl. All rights reserved. September 2020: EU/OTHR/M/20/0004. For the medical part of the virtual booth.

SOLVEON.