Cautionary Note Regarding Forward Looking Statements This presentation contains certain forward-looking statements about Curis, Inc. ("we," "us," or the "Company") within the meaning of the Private Securities Litigation

Corporate Presentation NASDAQ: CRIS

Cautionary Note Regarding Forward

Looking Statements This presentation contains certain forward-looking statements about Curis, Inc. ("we," "us," or the "Company") within the meaning of the Private Securities Litigation Reform Act of 1995, as

amended. Words such as "expect(s)," "believe(s)," "will," "may," "anticipate(s)," "focus(es)," "plans," "mission," "strategy,"

"potential," "estimate(s)", "intend," "project," "seek," "should," "would" and similar expressions are intended to identify forward-looking statements. Forward-looking statements are statements that are not historical facts,

reflect management's expectations as of the date of this presentation, and involve important risks and uncertainties. Forward-looking statements herein include, but are not limited to, statements with respect to the timing and results of

future clinical and pre-clinical milestones; the timing of future preclinical studies and clinical trials and results of these studies and trials; the clinical and therapeutic potential of our drug candidates; and management's ability to

successfully achieve its goals. These forward-looking statements are based on our current expectations and may differ materially from actual results due to a variety of important factors including, without limitation, risks relating to: whether any

of our drug candidates will advance further in the clinical development process and whether and when, if at all, they will receive approval from the U.S. Food and Drug Administration or equivalent foreign regulatory agencies; whether historical

preclinical results will be predictive of future clinical trial results; whether historical clinical trial results will be predictive of future trial results; whether any of our drug candidate discovery and development efforts will be successful;

whether any of our drug candidates will be successfully marketed if approved; our ability to achieve the benefits contemplated by our collaboration agreements; management's ability to successfully achieve its goals; the sufficiency of our cash

resources; our ability to raise additional capital to fund our operations on terms acceptable to us or the use of proceeds of any offering of securities or other financing; general economic conditions; competition; and the other risk factors

contained in our periodic and interim reports filed with the Securities and Exchange Commission which are available on the SEC website at www.sec.gov. You are cautioned not to place undue reliance on these forward-looking statements that speak only

as of the date hereof, and we do not undertake any obligation to revise and disseminate forward-looking statements to reflect events or circumstances after the date hereof, or to reflect the occurrence of or non-occurrence of any events, except as

Curis Mission & Strategy Developing

the New Generation of Targeted Cancer Drugs Translational Biology Clinical Development Mission Work relentlessly to develop innovative and differentiated therapeutics that improve the lives of cancer patients Strategy Selectthe right targets

Designthe right drugs Studythe right patients Design Execution Innovation People Precision Medicine

Company Overview Investment Thesis

Curis seeks to develop novel, first-in-class, cancer therapeutics that we believe have significant potential in areas of unmet patient need Robust Pipeline CA-4948:first-in-class inhibitor of IRAK4 in oncology There are no drugs currently approved

for IRAK4 inhibition in oncology CI-8993:first-in-class antagonist of VISTA There are no drugs currently approved for VISTA inhibition Corporate Experienced management team with proven capabilities Curis R&D pioneered the first-in-class

inhibitor of the Hedgehog pathway (Erivedge ) partnered with and commercialized by Genentech/Roche for advanced basal cell carcinoma Cash and cash equivalents of $26.3M as of Nov 30, 2020

Evolution of Curis Progressing through

Clinical Studies on the Path to Potential Registration Registrational Strategy Initiate Combination Study of CA-4948 and ibrutinib in NHL and evaluate potential paths for registration Report expanded Ph1 data for CA-4948 study in AML/MDS and

identify Recommended Phase 2 Dose (RP2D) Initiate the clinical and non-clinical research collaboration with the NCI under the CRADA for CA-4948 Report initial clinical data for CI-8993 Ph1 study targeting VISTA in solid tumors 2019 2020 2021 Expand

Clinical Opportunities Report expanded Ph1 data for CA-4948 study in NHL and identify Recommended Phase 2 Dose (RP2D) Initiate a Ph1 study of CA-4948 in AML/MDS including patients expressing IRAK4-L and report initial Ph1 data Acquire exclusive

option to license the leading VISTA monoclonal antibody program (CI-8993) and initiate a Ph1 study Initial Clinical Data Report initial Ph1 data for CA-4948 in NHL Evaluate new published research in IRAK4-L expression and the potential opportunity

for CA-4948 in AML/MDS

Indication Proof of Principle Safety

Dose Optimization Clinical Activity Pivotal Commercial Heme Malignancies CA-4948* IRAK4 MYD88/TLR-altered Lymphoma (NHL) CA-4948* IRAK4 IRAK4L-expressing Leukemia (AML/MDS) Fimepinostat HDAC/PI3K MYC-altered Cancers Immune Checkpoint Inhibitors

CI-8993** VISTA VISTA-expressing Cancers CA-327* PDL1/TIM3 PDL1/TIM3-expressing Cancers CA-170* PDL1/VISTA PDL1/VISTA-expressing Cancers Approved Drug Erivedge*** Hedgehog Basal Cell Carcinoma Pipeline All Curis programs are novel, first-in-class

CLINICAL MARKETED *IP licensed from Aurigene **Option to license IP from ImmuNext ***IP licensed to Genentech (Curis receives royalty income) 6 PRE-CLINICAL

IRAK4 Targeted Program in NHL CA-4948:

In development for treatment of cancers driven by NF-kB and the TLR/Myddosome

CA-4948 Overview Data from Curis

preclinical study Booher et al. AACR 2017 (poster #1168) Smith et al. Nat Cell Biol 2019 Profile Value Proposition First-in-class IRAK4 inhibitor in cancer Specific malignancies in Lymphoma are characterized by overactivity of NF-kB and

the TLR/myddosome (which is dependent upon IRAK4) Specific malignancies in Leukemia are characterized by spliceosome mutations that cause an overexpression of IRAK4-L (the oncogenic isoform of IRAK4) Composition-of-matter IP extends into 2035 Target

Patient Population Lymphoma: 100% of patients treated w/ibrutinib (IRAK4i combination with BTKi) Leukemia: >50% of AML/MDS patients (population which overexpresses IRAK4-L) Product Candidate Description Potent and orally bioavailable inhibitor of

IRAK4 for treatment of NF-kB driven lymphomas and IRAK4-L driven leukemia In Lymphoma: Potent suppressor of NF-kB signal transduction2 Phospho-protein levels in AML cells after treatment with CA-4948 Affinity Kinase Kd (nM) IRAK4 23 IRAK1 12,000

IRAK2 >20,000 IRAK3 8,500 Designed to be best-in-class IRAK4 inhibitor1 First-in-Class Inhibitor of IRAK4 in Oncology In Leukemia: >50% of AML/MDS patients overexpress IRAK4-L3 Unstimulated Control 10 1.0 0.1 mM P-IKKa/b P-NF-kB P-ERK

CA-4948 Novel Mechanism of Action for

Addressing NF- B Pathway is Oncogenic Pathway activates NF- B Pathway is dependent upon BTK Pathway is Oncogenic2,3,4 Pathway activates NF- B Pathway is dependent upon IRAK4 Signaling requires myddosome, which requires IRAK4 IMBRUVICA

Package Insert. Rev 08/2018 Ngo et al. Nature. 2011 Feb 3;470(7332):115-9 K ppers et al. J Exp Med. 2015. 212(13): 2184 Smith et al. Nat Cell Biol 2019 TLR1 B cell receptor Lymphoma1 (NHL) IRAK1 BTK CARD11 MALT1 BCL10 ibrutinib TLR2 TLR4 TLR5

TLR6 TLR7 TLR8 TLR9 Myddosome MYD88 CA-4948 IRAK4 BTK Pathway TLR Pathway Leukemia2 (AML/MDS) Endosome p65 p50 NF- B BTK and TLR are parallel pathways and primary independent activators of NF- B In Nov 2020, the NCI selected CA-4948 and

entered into a CRADA agreement with Curis to conduct non-clinical and clinical studies of CA-4948 as a potential anti-cancer agent that works via suppression of the TLR Pathway

CA-4948 in Lymphoma Trial Design

Study Objectives Primary: Safety and tolerability Secondary:Pharmacokinetic (PK) profile, preliminary anti-cancer activity Study Population Relapsed/Refractory disease Histopathologically confirmed B-cell NHL, including WM/LPL Age 18 years

ECOG performance status of 1 Dosing Oral, QD or BID continuous dosing 21-day cycles Dose Levels, 3+3 Design QD: 50, 100mg BID: 50, 100, 200, 300 or 400mg Baseline Characteristics of Ph1 Patients Overall (N=31) Male 26(84%) Female 5(16%)

Median Age 69yrs Histology Diffuse large B-cell lymphoma (DLBCL) 14(45%) Transformed follicular lymphoma (t-FL/DLBCL) 6(19%) Waldenstr m's Macroglobulinemia (WM) 4(13%) Other Lymphoma* 7(23%) Prior Therapies Median prior lines of

therapy 4 prior lines BTK inhibitor, n (%) 6(19%) CAR-T, n (%) 5(16%) ASCT , n (%) 7(23%) Other 13(42%) MYD88 Status Positive, n (%) 2(6%) Negative, n (%) 18(58%) Unknown, n (%) 11(35%) *includes Lymphoplasmacytic (n=2), Mantle Cell (n=2), Marginal

Zone (n=2), High Grade MYC-BCL6 (n=1) Data cut-off: 23Nov2020

CA-4948 in Lymphoma Two Potential

Biomarkers Identified NF- B phospho-p50 Positive expression of NF- B phospho-p50 indicates that the NF- B complex is active MYD88 Mutation Genetic alteration of MYD88 at baseline causes constitutive activation of the myddosome and is

a driver of NF- B activity Is NF- B activity driven by the TLR/myddosomal axis? Is NF- B is active? TLR1 B cell receptor Lymphoma1 (NHL) IRAK1 BTK CARD11 MALT1 BCL10 ibrutinib TLR2 TLR4 TLR5 TLR6 TLR7 TLR8 TLR9

Myddosome MYD88 CA-4948 IRAK4 BTK Pathway TLR Pathway Leukemia2 (AML/MDS) Endosome p65 p50 NF- B IMBRUVICA Package Insert. Rev 08/2018 Ngo et al. Nature. 2011 Feb 3;470(7332):115-9 This potential biomarker may support patient selection and

provide evidence that CA-4948 is hitting the direct target (IRAK4) and inhibiting the downstream target (the NF- B complex) This potential predictive biomarker may support patient enrichment by identifying patients with excessive myddosome

activity (who may therefore be good candidates for IRAK4 inhibition)

CA-4948 in Lymphoma Early Biomarker

Data from Phase 1 patients Patient Best Response 12-1002 +86% PD 018-2004 +156% PD 001-4002 +7% PD 002-4004 +75% PD 012-4004 +125% PD 012-5006 +190% PD 013-6001 +98% PD NEGATIVE at baseline NF B phospho-p50 expression before treatment with

CA-4948 Patient Best Response 19-1001 -35% SD 02-1001 -23% SD 02-3003 +22% SD 012-5007 -34% SD 002-6007 +25% SD 002-6008 +16% SD 15-1001 +66% PD POSITIVE at baseline NF B phospho-p50 expression before treatment with CA-4948 NF- B

phospho-p50 NF- B phospho-p50 protein expression at baseline (indicator of NF- B activity) correlates with patient outcomes Note: data included for all patients for whom pre/post samples were available as of Nov 23, 2020 Before After

NEGATIVE after treatment with CA-4948 POSITIVE at baseline (Day 20) Treatment with CA-4948 Phospho-p50 Expression in Pre/Post Tumor Biopsies Also Provides Evidence that CA-4948 is Hitting the Target (IRAK4) and Downregulating NF- B Activity

After treating the patient with CA-4948, their tumor no longer expresses NF- B phospho-p50 p-p50 Biomarker May Support Patient Selection Patients whose tumors do not exhibit NF- B activity may not be amenable to NF- B downregulation 7

of 7 patients testing negative at baseline experienced disease progression 2 of these patients were dosed at 200mg BID Patients whose tumors do exhibit NF- B activity may be amenable to NF- B downregulation 6 of 7 patients testing positive

for p-p50 at baseline achieved stable disease or tumor shrinkage 1 of these patients (012-5007) was dosed at 300mg BID MYD88 Biomarker May Support Patient Enrichment Both patients whose tumor tested positive for MYD88 mutation saw tumor reduction

Observed tumor reduction is consistent with our thesis that patients with MYD88-mutated tumors should benefit from IRAK4 inhibition This clinical study is ongoing, more data are needed to confirm these potential biomarkers

Demonstrated Anti-Cancer Activity

Objective Response observed at 300mg BID (RP2D) Demonstrated Dose Response Tumor burden decreased with each increase in dose CA-4948 in Lymphoma Anti-Cancer Activity and Dose Response in a Patient with Waldenstr ms Macroglobulinemia (WM) Note:

This WM patient is one of the two patients in the Ph1 study who tested positive for MYD88 (dotted line indicates ongoing treatment) Data cut-off: 23Nov2020

CA-4948 in Lymphoma In Updated Ph1

Data, 300mg BID (RP2D) Offered Best Balance of Tolerability and Anti-Cancer Activity 200mg BID or 400mg BID 300mg BID (RP2D) Clear Single Agent Anti-Cancer Activity at RP2D Tumor reduction 6 of 7 pts in a heavily pretreated population (4 prior lines

of therapy) Durable Tolerability Profile at RP2D Patients receiving 300mg BID have remained on therapy for extended periods of time (1 to 2 years) Data cut-off: 23Nov2020

CA-4948 in Lymphoma In Updated Ph1

Data, 300mg BID (RP2D) Offered Best Balance of Tolerability and Anti-Cancer Activity Patients Dosed at Recommended Ph2 Dose (300mg BID) Days on Study (dotted line indicates ongoing treatment) Data cut-off: 23Nov2020 Clear Single Agent Anti-Cancer

Activity at RP2D Tumor reduction 6 of 7 pts in a heavily pretreated population (4 prior lines of therapy) Durable Tolerability Profile at RP2D Patients receiving 300mg BID have remained on therapy for extended periods of time (1 to 2

CA-4948 in Lymphoma 2021 Plan:

Initiate Clinical Study in Combination Therapy (CA-4948 + ibrutinib) Days of Treatment vehicle ibrutinib Combination Therapy (CA-4948 + ibrutinib) CA-4948 Monotherapy 0 5 10 15 20 25 30 0 300 600 900 1200 1500 Mean Tumor Volume (mm3) SEM

Anti-Cancer Activity in Monotherapy and Combination Therapy in MYD88-altered DLBCL preclinical model (OCI-Ly10) Mechanism of Action Supports Combination CA-4948 potentially offers a novel mechanism for reducing NF- B activity by targeting the

TLR/myddosome (a parallel and complementary pathway to BTK) Clear Single Agent Anti-Cancer Activity Monotherapy anti-cancer activity demonstrated in both preclinical models and initial Ph1 data Clear Synergy with ibrutinib CA-4948 and ibrutinib show

clear synergy in preclinical models Next Step: initiate clinical study of CA-4948 and ibrutinib Booher et al. Waldenstrom Roadmap Symposium 2019

CA-4948 in Lymphoma (planned

combination study) Trial Design Study Objectives Primary: Safety and tolerability of CA-4948 in combination with ibrutinib Secondary:Pharmacokinetic (PK) profile, preliminary anti-cancer activity Study Population Relapsed/Refractory disease

Histopathologically confirmed B-cell NHL, including WM/LPL Age 18 years ECOG performance Status of 1 Dosing CA-4948 - Oral twice daily ibrutinib - Oral daily at labeled dose 21-day cycles 3+3 escalation design for CA-4948

(1st cohort will be 200mg BID) Additional Patient Cohorts to be Studied in Planned Expansion BTK-na ve, Marginal Zone Lymphoma (MZL) BTK-na ve, ABC-DLBCL BTK-na ve, Primary CNS Lymphoma (PCNSL) Patients with adaptive resistance to

IRAK4 Targeted Program in AML/MDS

CA-4948: In development for treatment of cancers driven by IRAK4-L

CA-4948 in AML/MDS Landscape of

Disease Targets in AML/MDS Non-targeted therapies administered in monotherapy have historically provided limited clinical benefit, especially in relapsed/refractory patients Targeted therapies (e.g., FLT3, IDH) have been limited by the size of their

respective target patient populations IRAK4-L is a novel target in AML/MDS and has been shown to be preferentially expressed in >50% of the AML/MDS patient population Disease Driver % of Patient Population IRAK4-L > 50%1 FLT3 25-30%2 TET2

10-20%3 IDH2 9-13%4 IDH1 6-10%4 CEBPA ~10%3 Smith et al. Nat Cell Biol 2019 Saygin, et al. J Hematol Oncol. 2017 Apr 18 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6142505/ DiNardo et al. N Engl J Med 2018

IRAK4-L provides a genetic link to

oncogenic immune signaling in AML/MDS CA-4948 in AML/MDS IRAK4-L is a Novel Target in AML/MDS Specific Genetic Mutations Drive the Expression of the Long Isoform of IRAK4 (IRAK4-L) Oncogenic IRAK4-L, which is driven by spliceosome mutations (incl.

SF3B1 and U2AF1), is preferentially expressed >50% of AML/MDS patients CA-4948 treatment appears to reduce leukemic blasts in patient-derived xenografts IRAK4-L is Oncogenic CA-4948 Directly Targets IRAK4 Direct inhibition of the protein

associated with disease (IRAK4) may offer accelerated regulatory path Blocking IRAK4-L appears to reduce the formation of leukemia colonies in preclinical studies Smith et al. Nat Cell Biol. 2019 Choudhary et al. AACR 2017

CA-4948 in AML/MDS Trial Design

Study Objectives Primary: Maximum tolerated dose and recommended Phase 2 dose Secondary:Pharmacokinetic (PK) profile, preliminary anti-cancer activity Study Population Relapsed/Refractory disease Histopathologically confirmed AML or High-Risk MDS

Age 18 years ECOG performance Status of 2 Dosing Oral 28-day cycles 3+3 escalation design (200mg BID, 300mg BID, and 400mg BID) Baseline Characteristics of Ph1 Patients Overall (N=6) Male (%) 5(83%) Female (%) 1(17%) Median Age

(range) 72 (32-84) Median Prior Therapies (range) 3 (1-4) Histology Acute Myelogenous Leukemia (AML) 4(67%) Myelodysplastic Syndrome (MDS) 2(33%) Data cut-off: 23Nov2020

CA-4948 in AML/MDS Monotherapy

Anti-Cancer Activity Observed in Early Ph1 Data Blasts Baseline Blasts Best Resp Change AML 005-2003 32% 26% -19% AML 005-2002 39% 25% -36% AML 003-1002 24% 9% -63% hrMDS 003-1003 4% 2% -50% hrMDS 003-1001 11% 2% -82% Marrow CR AML 005-2001 23% 1%

-96% Marrow CR 1st patient dosed in Q3 2020 Consistent reduction of Marrow Blasts across population (6 patients) 2 patients have achieved Marrow CR 300mg 300mg 200mg Normal Range 300mg 200mg 200mg Note:To achieve Marrow CR, a patient's blast