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Corporate Presentation June 2019

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Disclaimers This presentation contains “forward‐looking” statements that are based on the beliefs and assumptions and on information currently available tomanagement of Kadmon Holdings, Inc. (the “Company”). All statements other than statements of historical fact contained in this presentationare forward-looking statements. Forward‐looking statements include information concerning the initiation, timing, progress and results of clinicaltrials of the Company’s product candidates, the timing or likelihood of regulatory filings and approvals for any of its product candidates, andestimates regarding the Company’s expenses, future revenues and future capital requirements. In some cases, you can identify forward-lookingstatements by terminology such as “may,” “will,” “should,” “expects,” “plans,” “anticipates,” “believes,” “estimates,” “predicts,” “potential” or“continue” or the negative of these terms or other comparable terminology. There are important factors that could cause the Company’s actualresults to differ materially from those expressed or implied by the forward-looking statements, including those factors discussed under thecaption entitled “Risk Factors” in the Company’s filings with the U.S. Securities and Exchange Commission (“SEC”), including the Company'sAnnual Report on Form 10-K for the fiscal year ended December 31, 2018, and Quarterly Report on Form 10-Q for the quarter ended March 31,2019, filed pursuant to Section 13 of the Securities Exchange Act of 1934, as amended, with the SEC.

Forward-looking statements involve known and unknown risks, uncertainties and other factors that may cause the Company’s actual results,performance or achievements to be materially different from any future results, performance or achievements expressed or implied by theforward-looking statements. Forward-looking statements represent the Company’s beliefs and assumptions only as of the date of thispresentation. Although the Company believes that the expectations reflected in the forward-looking statements are reasonable, it cannotguarantee future results, levels of activity, performance or achievements. Except as required by law, the Company assumes no obligation topublicly update any forward‐looking statements for any reason after the date of this presentation to conform any of the forward-lookingstatements to actual results or to changes in its expectations.

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About Kadmon • Late-stage biopharma company headquartered in New York, NY (NYSE: KDMN) • Therapeutic focus areas:

– Inflammation and fibrosis

– Immuno-oncology (I-O)

Research Clinical Development Commercial Operation

• In-house drug discovery:

– KD033: Anti-PD-L1/IL-15 fusion protein for I-O

– KD045: ROCK inhibitor for fibrosis

• KD025 (ROCK2 inhibitor):

– FDA Breakthrough Therapy Designation and ongoing registration trial in cGVHD

– Ph2 trial in systemic sclerosis initiating 2Q 2019

• Generic product candidates for Wilson’s disease

• Supports development and future commercialization of Kadmon’s clinical pipeline

4

Kadmon: Upcoming Milestones Product Indication Milestone

KD025 (ROCK2 inhibitor)

Chronic Graft-Versus-Host Disease (cGVHD)

Complete enrollment in ongoing registration trial (2H 2019) Provide guidance on initial analysis of registration trial and

regulatory pathway (2H 2019)

Systemic Sclerosis (scleroderma) Initiate Phase 2 clinical trial (2Q 2019)

KD033 (anti-PD-L1/IL-15 fusion protein)

Immuno-oncology Submit Investigational New Drug (IND) application and initiate clinical trial (2H 2019)

KD045(pan-ROCK inhibitor) Fibrotic Diseases Submit IND application and initiate clinical trial (1H 2020)

KD034 (generic trientine

hydrochloride) Wilson’s Disease Continue dialogue with FDA regarding regulatory approval

5

ROCK Inhibition and KD025

66

KD025: Most Advanced Product Candidate KD025, an Oral, Selective ROCK2 Inhibitor

• Rho-associated coiled-coil kinase (ROCK) is a serine/threonine kinase – Mediates cell movement, shape, differentiation and function1

– Two isoforms exist: ROCK1 and ROCK21

• Kadmon research has helped define the role of ROCK in key areas, including: – Autoimmune and inflammatory diseases

– Fibrotic diseases

• KD025 is Kadmon’s oral ROCK2-selective inhibitor – More than 450 individuals have been treated with KD025 in ongoing and completed studies

– Well tolerated

– Demonstrated clinical activity at 200 mg

• KD025 has been granted FDA Breakthrough Therapy Designation and Orphan Drug Designation for the treatment of chronic graft-versus-host disease (cGVHD)

1Small GTPases. 2014; 5: e29846.

77

ROCK2 Plays Key Role in Autoimmune and Inflammatory Disease ROCK2 Inhibition Rebalances Immune Response to Treat Immune Dysfunction1,2

STAT3(Th17)

STAT5(Treg) Inflammation

Resolution Inflammation Resolution

STAT3(Th17)

STAT5(Treg)

ROCK2 Activation ROCK2 Inhibition

RORγtIRF4

• ROCK2 inhibition downregulates pro-inflammatory Th17 responses and increases Treg function, helping to resolve immune dysregulation

– Reduces STAT3 phosphorylation and increases STAT5 phosphorylation

• ROCK2 inhibition re-establishes immune homeostasis

1Proc Natl Acad Sci, 2014; 2Blood, 2016

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ROCK is an Intercellular Integrator of Pro-fibrotic SignalsROCK Regulates Multiple Pro-fibrotic Processes, Including Myofibroblast Activation

• ROCK is downstream of major pro-fibrotic mediators

• ROCK mediates stress fiber formation

• ROCK regulates transcription of pro-fibrotic genes

Stress fiber formation

ROCK

CTGFMKL1

MKL1

MKL1

Matrix stiffness

Myofibroblast Cell

Am J Pathol. 2015 Apr;185(4):909-12.

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KD025 Rebalances Th17/Tregs and Down-regulates B Cells

Research conducted by Jeff Bluestone, Ph.D., UCSF

Control DMSO KD025 0.3 µM 1 µM

IL-17 (Th17)

Control DMSO KD025 KD0250.3 µM 1 µM

KD025BM +T cells

(cGVHD)

BM KD025BM +T cells

(cGVHD)

BM

B cells

Flynn, Blazar et al, Blood 2016

Foxp3+ (Tregs)

%CD

4+PD

1Hi

CXCR

5+Fo

xp3-

%CD

19+

GL7

+Fa

sHi

%CD

4+PD

1Hi

CXCR

5+Fo

xp3+

Tfh cells Treg cells

KD025BM +T cells

(cGVHD)

BM

KD025 Reduces Pro-Inflammatory Th17 Cells (IL-17) and Increases Regulatory T Cells (Tregs)

KD025 Decreases Tfh and B Cells and Up-regulates Tregs, Helping to Resolve Inflammation

1010

KD025 Reduced Lung Fibrosis in Bleomycin Model

Intratracheal Bleomycin Day 0

0 8 21

KD025 treatment administered (orally, 50, 100 or 150 mg/kg QD)

Day:

Tissue Harvest Intratracheal Bleomycin

Vehicle or KD025Day 8

Normal Lung Pre-Treatment Lung

Treatment: Day 21

Control KD025 50 mg/kg QD

KD025 100 mg/kg QD

KD025 150 mg/kg QD

KD025 Treatment Administered on Day 8, When Fibrosis is Already Established

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KD025 in cGVHD

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Pathophysiology of Chronic GVHD (cGVHD) cGVHD is Driven by Immune Cells and Pro-inflammatory Cytokines

• cGVHD involves both T cells and B cells

– Overproduction of pro-inflammatory cytokines IL-21 and IL-17

– Over-activation of T follicular helper (Tfh) cells and B cells, leading to over-production of antibodies

– Deficiency of regulatory T (Treg) cells, leading to a lack of appropriate regulation of immune response

Blood, 2017

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cGVHD: ~14K Patients with Significant Unmet Need Estimated 14K Patients and Growing, with ~50% Progressing Through 3+ Lines of Therapy

• cGVHD prevalence: ~14,000 (U.S., 2017)

– 2015-2017 CAGR of 4%

• cGVHD incidence: ~5,200 (U.S., 2017)

– Growth consistent with that of HSCT transplants

• Patients cycle through lines of therapy, each line lasting ~3-4 months, reinforcing need for effective, well-tolerated therapy1

Sources: 2013- June 2018 IQVIA Pharmetrics commercial medical claims; 2008 – 2016 CMS Medicare Fee-for-Service medical claims (5% Non-Institutional Sample); Trinity KoL and Treater Interviews N=15 interviews; N=93 cGVHD Patient Charts; Chart study focused on patients with 3+ lines of treatment for cGVHD; Arai (2015); KD025 expected tx duration of >1 year, based on clinical efficacy and safety data as well as KOL feedback

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Phase 2a Trial of KD025 in cGVHD: Design and Key Endpoints

Cohort 1: 200mg QD

(n=17)

Cohort 2:200mg BID

(n=16)

Cohort 3:400mg QD

(n=21)

Three cohorts enrolled sequentially,following safety assessment of previous cohort

All data as of 13 September, 2018

Key Eligibility Criteria:

• Adults who have had allogeneic HCT with steroid-dependent or steroid-refractory cGVHD

• Have persistent active cGVHD after at least 2 months of steroid therapy

• Receiving glucocorticoid therapy +/- calcineurininhibitor therapy for cGVHD

• No more than 3 prior lines of treatment for cGVHD

Key Endpoints:• ORR, per 2014 NIH

criteria

• Safety and tolerability of KD025 in patients with cGVHD

• Duration of response (DOR)

• Response by organ system

• Changes in corticosteroid and calcineurin inhibitor dose

KD025-208: Phase 2a Study of KD025 for Patients with cGVHD

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KD025-208: Demographics and Baseline Characteristics Demographics and Baseline Characteristics Cohort 1

(n=17)Cohort 2

(n=16)Cohort 3

(n=21)Median age (years (range)) 50 (20-63) 55 (30-75) 46 (25-75)Male/Female (%/%) 76/24 56/44 57/43Median time cGVHD diagnosis to study (months) 25.9 15.8 20.3Organ Involvement

≥4 organs involved 8 (47) 10 (63) 8 (38)Eyes 14 (82) 11 (69) 17 (81)Skin 13 (76) 12 (75) 15 (71)Mouth 13 (76) 11 (69) 11 (52)Joints and fascia 12 (71) 11 (69) 10 (48)Lungs 3 (18) 3 (19) 11 (52)Upper GI 2 (12) 4 (25) 2 (10)Esophagus 2 (12) 0 (0) 5 (24)Lower GI 1 (6) 2 (13) 1 (5)Liver 0 (0) 2 (13) 0 (0)

Severe cGVHD1 12 (71) 14 (88) 16 (76)

Prior Therapies2 Cohort 1(n=17)

Cohort 2(n=16)

Cohort 3(n=21)

Median prednisone dose at BL (mg/kg/day) 0.22 0.19 0.16Prior lines of therapy

Median 3 2 2≥2 prior lines of therapy (n (%)) 15(88) 9(56) 12(57)

• 48% of all patients had ≥4 organs affected

– Included both inflammatory and fibrotic manifestations

• 67% of all patients had received ≥2 prior lines of cGVHD therapy

1Defined as at least 1 organ with NIH Activity Assessment score of 3, or lung score of 2 or 3, at baseline2ECP was not counted as a prior systemic therapy

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KD025-208: Safety and Tolerability

1 Headache; Diarrhea2 Relapse of Leukemia; Lung infection; Cardiac arrest. All considered not related to KD025

Safety Overview, n (%) Cohort 1(n=17)

Cohort 2(n=16)

Cohort 3(n=21)

ITT(n=54)

Median weeks of treatment 37 33 27 30Any Adverse Event (AE) 16 (94) 16 (100) 19 (90) 51 (94)Grade 3 / 4 AE 10 (59) 10 (63) 9 (43) 29 (54)SAE 5 (29) 6 (38) 9 (43) 20 (37)Drug related AE

Any related AE 6 (35) 9 (56) 9 (43) 24 (44)Related AE leading to discontinuation 2 (12)1 0 0 2 (4)Related Grade 3 / 4 event 2 (12) 4 (25) 2 (10) 8 (15)Related SAE 0 0 0 0

On study deaths 0 0 3 (14)2 3 (6)

Commonly Reported AEs, n (%) Cohort 1(n=17)

Cohort 2(n=16)

Cohort 3(n=21)

ITT(n=54)

All Grade, in ≥20%Upper respiratory tract infection 5 (29) 6 (38) 3 (14) 14 (26)ALT / AST increased 6 (35) 4 (25) 3 (14) 13 (24)Fatigue 5 (29) 3 (19) 5 (24) 13 (24)Nausea 6 (35) 2 (13) 5 (24) 13 (24)Diarrhea 6 (35) 2 (13) 4 (19) 12 (22)

Grade 3 / 4, in ≥5%GGT increased 3 (18) 3 (19) 0 6 (11)Hyperglycemia 2 (12) 0 2 (12) 4 (7)Anemia 2 (12) 1 (6) 0 3 (6)Dyspnea 1 (6) 1 (6) 1 (5) 3 (6)

• AEs were overall consistent with those expected in cGVHD patients receiving corticosteroids

• No treatment-related SAEs observed with KD025

• No apparent increased risk of infection

– No CMV infection reported

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KD025-208: Overall Response Rate (ORR) Responses Achieved Across Key Patient Subgroups

Cohort 1(n=17)

Cohort 2(n=16)

Cohort 3(n=21)

ORR 65%(11/17)

63%(10/16)

52%1

(11/21)

95% CI (41, 83) (39, 82) (32, 72)

1Three patients in Cohort 3 did not reach first response assessment. On a response-evaluable basis, Cohort 3 ORR = 61% (11/18)

ORR (ITT Population)

59% 58%62%

55%

0%

10%

20%

30%

40%

50%

60%

70%

80%

ITT ≥2 Prior lines of therapy ≥4 Organs Involved Severe cGVHD

Ove

rall

Res

pons

e R

ate

ITT (n=54)

≥4 organs involved (n=26)

Severe cGVHD (n=42)

≥2 prior lines of therapy (n=36)

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KD025-208: Duration of Response (DOR) Responses Achieved with KD025 Are Durable

• Responses were rapid: 75% of responders have achieved a response at the first assessment (8 weeks)

• Kaplan-Meier median DOR of 28 weeks in ITT responder population

• 22% of all patients have remained on KD025 therapy for >1.5 years1

• Data continue to mature

1As of March 2019

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• 7 patients have completely discontinued steroids

• Steroid dose reductions observed in responders and non-responders

• Tacrolimus dose reductions observed

KD025-208: Corticosteroid and Tacrolimus Dose Reductions

Cohort 1 (%) Cohort 2 (%) Cohort 3 (%)

% reduction in median corticosteroid dose 44% 23% 10%

Patients with corticosteroid dose reduction 13/17 (76) 9/16 (56) 15/21 (71)

Corticosteroid discontinuations 4/17 (24) 1/16 (6) 2/21 (10)

69% of Patients Have Reduced or Discontinued Steroids and other Immunosuppressants

2020

KD025-208: Pharmacodynamics KD025 May Modulate Immune Homeostasis by Restoring the TH17/Treg Balance

• With KD025 treatment:

– Treg cells increased

– TH17 decreased

• Consistent with KD025 mechanism of action

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KD025-208: Conclusions

KD025 was Well Tolerated and Achieved Clinically Meaningful Responses

• KD025 was well tolerated:

– No treatment-related SAEs

– No increased risk of infection observed

• ORRs of ~60% across all three cohorts

– Responses observed in all affected organ systems, including in organs with fibrotic disease

• Durable and clinically meaningful responses:

– 69% of patients were able to reduce or discontinue corticosteroids and other immunosuppressants

– 72% of responders experienced clinically meaningful improvement (LSS score)

• PD data showed a decrease in TH17 and an increase in Treg cells during treatment with KD025

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• Open-label, two-arm trial with two doses of KD025 (200 mg QD and 200 mg BID) • Primary endpoint: ORR

– Clinical significance is achieved if ≥30% ORR in either study arm – Statistical significance is achieved if lower bound of 95% CI excludes <30% ORR

KD025-213: Ongoing Registration Trial of KD025 in cGVHD

KD025 200 mg BID(n=63)

KD025 200 mg QD(n=63)

Treat to progression

Primary Endpoint:• ORR, per 2014 NIH criteria

Key Secondary Endpoints: • Safety

• Duration of response

• Response by organ system

• Lee Symptom Score

• Changes in corticosteroid and calcineurin inhibitor dose

R

Key Eligibility Criteria:• Adults who have

had allogeneic HCT

• Active cGVHD

• Received ≥2 prior lines of systemic therapy for cGVHD

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KD025-213 Study Status Registration Trial of KD025 in cGVHD (KD025-213)

• FDA Breakthrough Therapy Designation for KD025 in cGVHD granted October 2018

• FDA Type B Breakthrough Therapy Meeting held in May 2019

– FDA remains aligned with Kadmon on registration study design and broader data package to support a potential New Drug Application (NDA)

• Anticipated 2H 2019 milestones:

– Complete enrollment in ongoing registration trial

– Provide guidance on initial analysis of registration trial and regulatory pathway of KD025 in cGVHD

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KD025: Additional Clinical Development

• Chronic multi-system disease characterized by skin thickening and organ fibrosis

• Affects 75,000 to 100,000 people in the United States1

• Double-blind, placebo-controlled, 60-patient Phase 2 trial of KD025 in systemic sclerosis initiating 1H 2019

– Primary endpoint: Combined Response Index for Systemic Sclerosis (CRISS) score 1American College of Rheumatology, 2017

KD025: Planned Phase 2 Clinical Trial in Systemic Sclerosis (Scleroderma)

KD025: Demonstrated Proof of Concept in Idiopathic Pulmonary Fibrosis (IPF)

• KD025 demonstrated clinical activity and tolerability in ongoing Ph2 proof-of-concept clinical trial

• Trial expanded to include an additional ~40 patients

• Data to support the development of Kadmon’s novel ROCK inhibitors for fibrotic diseases

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IL-15-Focused Biologics Platform

2626

Kadmon is Developing IL-15-Containing Fusion Proteins for I-O• Kadmon’s approach: Develop IL-15-containing fusion proteins to target I-O non-responders and

enhance durability of response

– Localized IL-15 stimulation of NK, NKT and CD8+ memory T cells should overcome resistance, promote efficacy and induce long-lasting responses compared to existing combination therapies

– Targeted IL-15 activity to tumor microenvironment to mitigate safety concerns

• Lead candidate: KD033, an anti-PD-L1/IL-15 fusion protein, entering the clinic 2H 2019

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• Demonstrated efficacy in multiple syngeneic mouse models • Significantly inhibited tumor growth in PD-L1-expressing murine models resistant to approved I-O therapies • Induced immune system memory

– KD033 surrogate-treated MC38 colon adenocarcinoma mouse model survived tumor rechallenges

Lead I-O Candidate KD033 Entering the Clinic 2H 2019 KD033 (anti-PD-L1/IL-15 Fusion Protein) Targets IL-15 Activity to Tumor Microenvironment

Perc

ent S

urvi

val

Rechallenge

***

n = 12 per group

Rechallenge

Day 77 Day 142

tumor ~80 mm3

Dosing once a week

100% tumor free post rechallenge

1D7A8: Anti-PD-L1 antibody in KD033 surrogate, without IL-152KD033 surrogate recognizes human, NHP, rat and mouse PD-L1

KD033 surrogate 3.3 mg/kg IP QWx42

D7A8 10 mg/kg IP QWx41

Vehicle

Days Post Inoculation

2828

• KD033 + anti-PD-1 demonstrated strong anti-tumor activity (6/10 tumor-free mice) and long-term durability (180+ days)

• Tumor-free mice generated memory response to the original tumor (CT26) and also rejected a different tumor (EMT6; breast) (epitope spreading)

• KD033 surrogate + anti-PD-1 resulted in only a transient body weight decrease (<10%), suggesting acceptable safety

KD033 Combined with Anti-PD-1 Induced Synergistic Efficacy

**

Perc

ent S

urvi

val

Mean Tumor Growth Body Weight CT26 (Colon)

Log-rank (Mantel Cox) test: *** p<0.001

TGI at d30

****

t test: **** p<0.0001, * p<0.05

Anti-PD1 RMP1-14, BIWx3

tumor ~100mm3

KD033 Surrogate, IV

aPD1 treatments

6/10 tumor-free mice***

Days Post Inoculation100

t test: ** p<0.01

*

180140

Rechallenge: CT26 CT26 and EMT6

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KD045: ROCK Inhibitor for Fibrosis

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KD045: ROCK Inhibitor Candidate for Fibrosis KD045 Entering the Clinic in 1H 2020

hinge

Activationloop

G-loop

• Kadmon has identified and developed proprietary, next-generation ROCK inhibitors for fibrotic diseases

• KD045: Lead candidate entering the clinic 2H 2019 – Enhanced potency and AGC-kinase activity – Selectively targets ROCK, exhibiting favorable safety profile

• KD045 inhibited key fibrotic processes in multiple in vivo pharmacology models: • Lung fibrosis• Kidney fibrosis• Liver fibrosis

Earlier-generation ROCK inhibitors target the majority of the AGC kinase family and lack specificity or potency to effectively target ROCK

AGC Kinase Family

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Commercial Operation

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Kadmon Pharmaceuticals: Commercial Operation Specialty-Focused Commercial Operation

• Kadmon Pharmaceuticals is our wholly-owned subsidiary

• Supports development and future commercialization of Kadmon’s clinical product candidates

– Expertise in product launches and commercial growth in rare diseases and specialty distribution channels

– Capabilities include regulatory, quality assurance, supply chain/logistics, pharmacovigilance, marketing and business analytics

Kadmon commercial infrastructure based in Warrendale, PA

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KD034 for Wilson’s Disease

1American Liver Foundation, 2018; 2For up to 30 days

KD034: Generic Product Candidate for Wilson’s Disease

• Wilson’s Disease: Genetic disorder characterized by excess copper accumulation

– 10,000 in the United States are affected by WD1

• KD034: generic formulation of trientine hydrochloride for WD

• Two ANDAs submitted to the FDA for KD034 (bottle and blister pack)

– Blister pack offers room temperature stability2

• Kadmon is in dialogue with the FDA regarding regulatory approval for KD034

– Kadmon will leverage its commercial operation to market KD034, if approved

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Financial Profile

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Financial ProfileKDMN Financial Summary

• Cash and cash equivalents of $99.4 million as of March 31, 2019

• ~10.7% ownership1 of MeiraGTx (Nasdaq: MGTX), a clinical-stage gene therapy company

• 129,479,895 common shares outstanding as of May 3, 2019

• Trades on the NYSE under the ticker symbol “KDMN”

1As of March 31, 2019