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

CA-4948 & CI-8993 Clinical Data

Update January 2022 Exhibit 99.1

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, expectations of the potential for Company's

proprietary drug candidates CA-4948 and CI-8993, including with respect to the potency, anti-cancer activity, durability and tolerability of CA-4948 and CI-8993; future studies with respect to CA-4948 and CI-8993; the potential advantages and

benefits of CA-4948, CI-8993 and checkpoint inhibitors over other therapies; and the Company's plans to advance its development programs for CA-4948 and CI-8993, including with respect to anticipated results, clinical trials, regulatory and

commercialization plans and timelines. 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 required by law.

Today's Participants James

Dentzer President & Chief Executive Officer at Curis Robert Martell, MD, PhD Head of R&D at Curis Daniel DeAngelo, MD, PhDChief, Division of Leukemia at Dana-Farber Cancer Institute

Introductory Remarks Clinical update on

CA-4948 (IRAK4) and CI-8993 (VISTA) CA-4948 addresses a novel target (IRAK4) and: (1) demonstrates clear anti-cancer activity as an oral single agent (2) is active in genetically-defined populations that can be identified and enrolled (3) has the

added potential benefit of also hitting FLT3 CI-8993 addresses a novel target (VISTA) and: (1) has successfully cleared dose level where Janssen observed dose-limiting toxicity (DLT) (2) with pharmacodynamic effects suggesting multiple anti-cancer

mechanisms are being activated

CA-4948: First-in-class IRAK4 Inhibitor

Targeting Specific Genetic Populations in R/R AML and high-risk MDS (MDS)

Biology and CA-4948 Role of IRAK4 in

AML/MDS (normal vs. oncogenic activity) 1. Smith et al. Nat Cell Biol 2019. 2. Guillamot et al. Nat Cell Biol 2019. constitutive activation MYD88 IRAK1 IRAK4-S Myddosome IRAK1 IRAK4-L MYD88 Malignant Heme Cell2 Spliceosome Spliceosome Normal Heme

Cell1 Spliceosome Mutation CA-4948 CA-4948 Leukemia1 (AML, MDS) NF- B MAPK (normal immune signaling) IRAK4-L activity leads to NF- B IRAK4-S activity leads to MAPK Specific genetic mutations (SF3B1, U2AF1) in the spliceosome drive

overexpression of IRAK4-L IRAK4-L then causes constitutive activation of the myddosome, leading to overactivity of NF- B

CA-4948 is the Leading IRAK4 Inhibitor

in Development for Cancer Targeted design offers added potential benefit of also hitting FLT3 CA-4948 Kinase Interaction Map % Inhibition at 0.1 nM Illustration reproduced courtesy of Cell Signaling Technology CA-4948 binds specifically and with

high affinity to IRAK4 CA-4948 "fingerprint" illustrates unique molecular signature specifically engineered to hit key oncogenic targets Target Kd nM IRAK1 12,000 IRAK2 >20,000 IRAK3 8,500 IRAK4 23 DYRK1A 25 FLT3 wt FLT3 (D835H) 31 5

FLT3 (D835V) 44 FLT3 (D835Y) 3 FLT3 (ITD) 8 FLT3 (K663Q) 47 FLT3 (N841I) 16 Haspin (GSG2) 32 CLK1 10 CLK2 20 CLK3 >20,000 CLK4 14 TrkA 130 CA-4948 Binding Affinity DiscoverX Kinase Panel (378 kinases screened) Dual targeting of IRAK4 and FLT3

confers a potential efficacy advantage vs. other IRAK4 inhibitors and expands potential to additional genetic populations

Clinical Study Overview Phase 1/2 Study

CA-4948 in AML and MDS Study Objectives

1 : Determine maximum tolerated dose Determine recommended Phase 2 dose 2 :Pharmacokinetic (PK) profile Preliminary anti-cancer activity Study Population Relapsed/Refractory AML or high-risk MDS ECOG performance Status of 2 Age

18 years Dosing Oral, Twice Daily (BID) Dosing 28-day cycles Open-label, single arm, Phase 1/2 dose escalation and expansion study Data extraction date: Dec 16, 2021 1. These are non-targeted patients, due to lack of Spliceosome or FLT3

mutation, this population will be addressed in the combination therapy study; 2. One patient was not response evaluable because of discontinuation due to patient decision; 3. Two AML patients have both a spliceosome and FLT3 mutation and are

included in both populations (there are 13 total evaluable patients with Spliceosome or FLT3 mutation) Dose Escalation: 200/300/400/500 mg BID Dose Expansion: 300 mg BID 49 Total Patients Treated 43 Patients Started Treatment prior to September 30,

2021 AML Spliceosome2,3 (n=6) MDS Spliceosome (n=7) AML FLT33 (n=3) Jan 2022 Safety Update Jan 2022 Efficacy Update AML/MDS w/o targeted mutations1 (n=29)

Well-Tolerated and Manageable AE

Profile for CA-4948 in AML/MDS with No Cumulative Toxicities Observed No Grade 4 or 5 TRAEs reported; all AEs were manageable Data extraction date: Dec 16, 2021. 1. Data for the two patients that have escalated from 300 mg BID to 400 mg BID were

included in the 400 mg BID dose group. Grade 3+ Treatment-Related Adverse Event 200 mg BID (N = 3) 300 mg BID (N = 26) 400 mg BID (N = 17) 500 mg BID (N = 3) Preferred Term n (%) n (%) n (%) n (%) Number of patients having grade 3+ treatment-related

AEs 1 (33.3) 6 (23.1) 6 (35.3) 2 (66.7) Alanine aminotransferase increased 1 (33.3) 0 0 0 Blood creatine phosphokinase increased 0 1 (3.8) 0 0

Dizziness 1 (33.3) 0 0 0 Dyspnoea 0 0 1 (5.9) 0 Enterobacter infection 0 0 1 (5.9) 0 Fatigue 0 0 1

(5.9) 0 Gastrointestinal haemorrhage 0 1 (3.8) 0 0 Hypophosphataemia 0 1 (3.8) 0 0 Hypotension 0 1 (3.8) 0 0

Lipase increased 0 2 (7.7) 0 0 Platelet count decreased 0 1 (3.8) 0 0 Presyncope 0 0 1 (5.9) 0 Rhabdomyolysis 0

1 (3.8) 2 (11.8) 1 (33.3) Syncope 0 0 0 1 (33.3) No dose-limiting myelosuppression reported, which is a life-threatening problem characteristic of many cancer treatments, making CA-4948 favorable for

combinations Well-tolerated and manageable AE profile with no cumulative toxicities reported Recommended Phase 2 Dose

Clinical Data Overview: Three

Targeted Patient Populations (1) AML Spliceosome, (2) MDS Spliceosome, (3) AML FLT3

Heavily Pretreated Patient

Population Baseline Characteristics of AML/MDS Subsets AML Spliceosome1 (n=6) MDS Spliceosome (n=7) AML FLT31 (n=3) Female n (%) : Male n (%) 0 (0) : 6 (100) 5 (71) : 2 (29) 0 (0) : 3 (100) Age (yrs): median (range) 76 (60, 84) 74 (61, 80) 80

(78, 87) ECOG: n 0/1/2 0/4/2 2/5/0 0/1/2 Median platelets (103/mm3) (range) 28 (21, 80) 16 (7, 146) 21 (9, 23) Median ANC (103/mm3) (range) 0.23 (0, 3.3) 1.85 (0.15, 11.0) 0.05 (0, 0.11) Median lines of prior therapy (range)

2.5 (1, 4) 2 (1, 4) 2 (1, 4) Risk Category (ELN): Favorable / Intermediate / Adverse 0/3/3 NA 0/1/2 IPSS-R: Low / Intermediate / High / Very High NA 0/0/2/5 NA Prior therapy, n (%) HMA2 6 (100) 7 (100) 3 (100) Chemotherapy3 3 (50) 0 (0)

1 (33) Venetoclax 4 (67) 1 (14) 3 (100) Data extraction date: Dec 16, 2021. 1. Two AML patients have both a spliceosome and FLT3 mutation and are included in both populations (there are 13 total

evaluable patients with Spliceosome or FLT3 mutation); 2. HMA includes azacitidine, decitabine, and guadecitabine; 3. Chemotherapy includes cytarabine. Patient demographics indicate older population with poor prognosis; all patients received prior

hypomethylating agent (HMA) therapy

Encouraging Clinical Activity in R/R

AML/MDS Patient Populations CA-4948 shows activity as a monotherapy in patients with Spliceosome and FLT3 mutations Population #1: AML Spliceosome Patients1 CR/CRh Rate 2/5(40%) CR 1/5(20%) CRh 1/5(20%) Population #2: MDS Spliceosome Patients

Objective Response Rate (ORR) 4/7(57%) CR 0/7(0%) mCR 4/7(57%) Population #3: AML FLT3 Patients1 CR/CRh Rate 1/3(33%) CR 1/3(33%) CRh 0/3(0%) Data extraction date: Dec 16, 2021. 1. Two AML patients have both a spliceosome and FLT3 mutation and

are included in both populations (there are 13 total evaluable patients with Spliceosome or FLT3 mutation). Response criteria per 2017 ELN Criteria for AML and Modified IWG Criteria for MDS: CR=Complete Remission CRh=CR with partial hematologic

recovery mCR=marrow CR The CR and CRh patients are both MRD-negative 1 mCR patient went to Stem Cell Transplant (SCT) FLT3 mutation eradicated in 2 out of 3 patients Best Response Efficacy

Clinical Data: R/R AML Patients with

Spliceosome Mutation Patient Population #1

Unmet Need for R/R AML Patients with

Spliceosome Mutation Spliceosome mutations occur in ~10% of AML patients1 These mutations create a chronic inflammatory marrow microenvironment2, which impairs hematologic recovery3 Ability to achieve CR is impaired in patients with U2AF1/SF3B1

mutation4 There are no effective therapies for patients R/R to Ven/HMA: no unified standard of care No approved targeted therapies and no unified standard of care for these patients 1. DiNardo et al, Hematology Am Soc 2016; 2. Smith et al. Nat Cell

Biol 2019; 3. Trowbridge JEM 2021. Ochi Cancers 2021. Hou, Oncotarget 2016; 4. Hou, Oncotarget 2016; 5. Maiti et al. Haemtologica 2021 Opportunity to meaningfully improve outcomes in R/R AML patients with spliceosome mutations Intensive Elderly /

Non-Intensive Induction Chemo SCT Ven/HMA Ven/HMA No Effective Therapies (mOS 2-4 months5) Salvage chemo SCT Salvage chemo

Initial CA-4948 Data Compare

Favorably to Existing Therapies Potential to meaningfully improve outcomes in R/R AML patients with spliceosome mutation 1. CancerMPact Treatment Architecture U.S. AML, Cerner Enviza, www.cancermpact.com, accessed January 3, 2022. Excludes

Investigational Therapies; 2. Product Package Insert; 3. Ritchie et al, Leuk Lymphoma 2013; 4. Itzykson et al, Leuk Res 2014; 5. Frikha et al, Bulletin du Cancer 1996; 6. Gemtuzumab ozogamicin is only approved for patients with newly-diagnosed

CD33-positive AML or R/R CD33-positive AML Azacitidine2,4 LoDAC5 HMA Chemotherapy 17% CR/CRi rate Myelosuppressive IV or SC Administration ~13% ORR Myelosuppressive and Black Box Warning IV Administration Most Commonly Used in R/R AML with Wild Type

FLT3/IDH1 Decitabine2,3 HMA ~16% CR rate Myelosuppressive IV Administration >6 months on CA-4948 for patients with CR/CRh CA-4948 40% CR/CRh rate (2 of 5 patients) No dose-limiting myelosuppression Oral Administration Gemtuzumab Ozogamicin2,6

Monoclonal Anti-CD33 Antibody (ADC) ~26% CR Myelosuppressive and Black Box Warning IV Administration IRAK4 Inhibitor Initial CA-4948 data compare favorably vs. historical responses with mainstay treatments for R/R AML patients with wild type

Encouraging Clinical Activity in R/R

AML Patients with Spliceosome Mutation Achieved 40% CR/CRh rate, with treatment duration >6 months to date in responding patients CA-4948 achieved CR/CRh responses, despite transformed AML being historically highly resistant to treatment CR CRh

Dx Dose (BID) Risk Category (ELN) Baseline Molecular Mutations Prior Therapies Duration on CA-4948 (mos) Blasts Baseline Blasts Best Response % Change # Lines Therapy sAML 300 mg Intermediate RUNX1, WT1, SF3B1 1 decitabine 7 23 0 -100% (CRh) sAML

300 mg Intermediate U2AF1, FLT3, BCOR, WT1 1 decitabine/venetoclax 6+ 39 4 -90% (CR) AML 300 mg Intermediate U2AF1, NRAS 4 cytarabine/idarubicin, decitabine/venetoclax, fludarabine/cyclophosphamide/methotrexate, azacitidine 2.5 33 16 -52% AML 300 mg

Adverse FLT3, SF3B1, NRAS, PTPN11, RAD21, RUNX1, TET2, GATA, STAT3 4 cytarabine/daunorubicin, decitabine, decitabine/venetoclax, gilteritinib 2.6 95 77 -19% sAML 400 mg Adverse SF3B1, DNMT3A, P53 1 azacitidine/venetoclax 2 20 23 15% Data extraction

date: Dec 16, 2021; "+" in Duration of Treatment indicates the patient remains on treatment as of the date of data extraction. 1. Two AML patients have both a spliceosome and FLT3 mutation and are included in both populations (there

are 13 total evaluable patients with Spliceosome or FLT3 mutation).

Clinical Data: R/R MDS Patients with

Spliceosome Mutation Patient Population #2

Spliceosome Mutations Common in MDS

Spliceosome mutations (U2AF1/SF3B1) are the most prominent mutations in MDS, accounting for ~30% of all MDS patients1 These mutations create a chronic inflammatory marrow microenvironment2, which impairs hematologic recovery3 There are no effective

therapies for patients R/R to HMA: chemotherapy is standard of care Large unmet need for R/R MDS patients with spliceosome mutation 1. Ochi Cancers 2021.; 2. Smith et al. Nat Cell Biol 2019.; 3. Trowbridge JEM 2021. Ochi Cancers 2021.; 4. Jabbour et

al Cancer 2010; Prebet et al., JCO 2011; Duong et al, Clin Lymphoma Myeloma Leuk, 2013. Current standard of care offers limited therapeutic benefit to patients SCT Eligible Not SCT Eligible HMA SCT HMA No Effective Therapies (mOS 4-6

Relapsed/Refractory MDS Current standard of care offers little therapeutic benefit to patients 1. CancerMPact Treatment Architecture U.S. AML, Cerner Enviza, www.cancermpact.com, accessed January 3, 2022. Excludes Investigational Therapies; 2.

Pr bet et al, JCO 2011.; 3. Product Package Insert.; 4. Jabbour et al Cancer 2010; Pr bet et al., JCO 2011; Duong et al, Clin Lymphoma Myeloma Leuk, 2013. Chemotherapy2 Decitabine3 Azacitidine3 CA-4948 Chemotherapy HMA HMA IRAK4 Inhibitor

~8% ORR Myelosuppressive and Black Box Warning IV Administration 2nd line response data unavailable Myelosuppressive IV Administration 2nd line response data unavailable Myelosuppressive IV or SC Administration 57% mCR rate (4 of 7 patients, incl. 1

that went to SCT) No dose-limiting myelosuppression Oral Administration Initial CA-4948 data compared favorably vs. historical responses with the mainstay treatment for R/R MDS patients In MDS post-HMA mOS is 4-6 months4; clear unmet need for

these patients Most Commonly Used Therapies in R/R MDS1

Dx Dose (BID) IPSS-R Baseline

Molecular Mutations Prior Therapies Duration on CA-4948 (mos) Blasts Baseline Blasts Best Response % Change # Lines Therapy MDS 200 mg Very High Risk U2AF1 ,ASXL1, NF1, PHF6, GFI1, KDM6A, TET2 1 azacitidine 5.7 11 2 -82% (mCR) MDS 300 mg Very High

Risk U2AF1, DNMT3A, BCOR, STAG2, BCORL1, ETV6, SETBP1 1 magrolimab/azacitidine 3.3+ 12 5 -58% (mCR) MDS 400 mg Very High Risk SF3B1, RUNX1, NFE2 2 lenalidomide, guadecitabine 4.3 7 3 -57% (mCR) MDS 300 mg High Risk SF3B1, DNMT3A, ASXL1, TET2, EZH2 2

azacitidine, canakinumab 0.9 8 4 -50% (mCR) MDS 300 mg High Risk U2AF1, ASXL1 4 lenalidomide, azacitidine, cyclosporine, decitabine 5.3+ 3 2 -33% MDS 300 mg Very High Risk SF3B1, ASXL1, NF1, SH2B3, RUNX1, PHF6, CBL, GFI1, EZH2 3

ipilimumab/azacitidine, quizartinib/azacitidine, azacitidine/venetoclax/ pevonedistat 1.6 8 9 13% MDS 400 mg Very High Risk U2AF1, ASXL1, BCOR, DNMTA, GATA2, SETBP1 1 azacitidine 1.2 9 62 >100% Encouraging Clinical Activity in R/R MDS Patients