Slide 1: October 2020
OCTOBER 2020
Slide 2: Forward Looking Statements and Disclaimers
FORWARD LOOKING STATEMENTS AND DISCLAIMERS Page | 2 Disclaimer : This presentation (“Presentation”) has been prepared to assist interested parties in making their own evaluation with respect to a potential business combination between Nuvation Bio, Inc. (“Nuvation Bio”) and Panacea Acquisition Corp.
Slide 3: Nuvation Bio – Summary
▪ Tackling the greatest unmet needs in oncology ▪ Experienced biotech leadership team led by David Hung, which successfully developed major oncology drugs including Xtandi ( $ 3 . 7 B in 2019 sales) and Talzenna ▪ Broad & validated wholly - owned pipeline with strong IP protection — Up to 6 INDs in
Slide 4: Nuvation Management Team and Board of Directors
Pag e | 4 DAN WELCH Former Chairman and CEO, InterMune ROBERT BAZEMORE CEO, Epizyme KIM BLICKENSTAFF Executive Chairman and Director, Tandem Diabetes Care MICHELLE DOIG Partner and Head of Corporate Development, Omega Funds Kate FALBERG Former CFO, Jazz Pharmaceuticals CLAUDIO NESSI, Ph.D . Investme
Slide 5: Deep Pipeline in Multiple Oncology Indications
DEEP PIPELINE IN MULTIPLE ONCOLOGY INDICATIONS Best - in - class wholly - owned pipeline with potential for exponential value appreciation Program Product Ca n d id ate Potential Indication(s) Preclinical Phase 1 Next Milestone CDK 2/4/6 NUV - 422 High - grade Glioma Metastatic Brain Tumors ER+ MBC
Slide 6: NUV-422 | CDK 2/4/6 Inhibitor
GBM ER+ mBC mCRPC Metastatic Brain Tumors 1Q21 FPI 1H22 Initiate Ph1 2H22 Initiate Ph1 4Q22 Initiate Ph1 NUV - 422 | CDK 2/4/6 Inhibitor
Slide 7: CDK2 Drives Resistance to CDK4/6 Inhibitors
CDK2 DRIVES RESISTANCE TO CDK4/6 INHIBITORS Tumors respond to CDK4/6 inhibition by signaling through CDK2, driving resistance Selectively targeting CDK2 in addition to CDK4/6 may prevent or reverse resistance Addressing Resistance CDK4/6 Inhibitors Three approved CDK4/6 inhibitors CDK4/6 class achie
Slide 8: NUV-422: Potent Inhibitor of CDK2/4/6
NUV - 422 has good drug - like properties 1 st Generation CDK 4 CDK 6 CDK 2 2 2 10000 4 2 2470 2 10 504 CDK 1 10000 10000 1627 2 nd Generation CDK 4 CDK 6 CDK 2 CDK 1 PF - 06873600 2 4 0.3 2 NUV - 422 2 1 7 73 NUV - 422: POTENT INHIBITOR OF CDK2/4/6 ▪ Target selectivity ▪ Good oral PK ▪ Good CYP pro
Slide 9: CDKN2A Role in Primary High-Grade Gliomas
Pag e | 9 With loss of p16 and p21 (via loss of p14) CDK2/4/6 is activated p14 and p16 are products of the CDKN2A gene CDKN2A ROLE IN PRIMARY HIGH - GRADE GLIOMAS CDKN2A Gene CDKN2A Deletion is Associated With Worse Survival (1) CDK2 Expression Is Associated With Lower Overall Patient Survival (2) (
Slide 10: NUV-422 Preclinical Tumor Inhibition in GBM Model
▪ NUV - 422 inhibits tumor growth far better than SOC temozolomide in glioblastoma xenograft model NUV - 422 PRECLINICAL TUMOR INHIBITION IN GBM MODEL Tumor Volume 0 5 10 15 20 25 0 200 400 600 Da y s Tumor Volume (mm 3 ) Vehicle NUV - 422 10mpk, PO, QD NUV - 422 30mpk, PO, QD NUV - 422 60mpk, PO, Q
Slide 11: High Concentrations of NUV-422 in the Brain
HIGH CONCENTRATIONS OF NUV - 422 IN THE BRAIN Page | 11 Dose ( mg/ k g ) Brain Conc (nM) Plasma Conc (nM) Brain / P la s m a Ratio 30 4096 375 11 100 5827 506 12 NUV - 422 Concentration Six Hours Post Dose (Rat) ~12X Higher Exposure in Brain vs Plasma
Slide 12: NUV-422-02: Seamless Phase 1/2 Trial Design
Ph2 Dose Expansion in CDKN2A Deleted Patients Ph1 Dose - Escalation in Unselected Population Select RP2D Page | 12 Cohort…. n Cohort 4 Cohort 3 Cohort 2 Cohort 1, 25 mg QD EXPANSION COHORT 1 CDKN2A deleted relapsed/refractory high - grade glioma (up to 40 pts) with measurable disease O B J E C T I V
Slide 13: Additional NUV-422 Opportunities in Tumors Which Metastasize to Brain
Tumor Types with Brain Mets Breast Colon NSC L C Melanoma CDKN Deleted Solid Tumors (e.g., pancreas) ▪ Potent, low nanomolar IC 50 s seen in tumor types that commonly metastasize to brain Cell Proliferation (IC 50 nM) 0 250 500 750 1 , 000 1 , 250 1 , 500 1 , 750 2 , 000 BEYOND PRIMARY BRAIN TUMORS,
Slide 14: CDK Inhibitors Dominate the ER+ Breast Landscape
CDK INHIBITORS DOMINATE THE ER+ BREAST LANDSCAPE $8B Surgery & Radiation Adjuvant Therapy 1L Metastatic 2L+ Metastatic Salvage Tx Hospice $25B Page | 14 ~500K Patients Annually $4B Positive Ph3 Data from MONARCH - E trial for abemaciclib at ESMO20 suggests role for CDK4/6 inhibitors in adjuvant ER+
Slide 15: NUV-422 Superior to Fulvestrant in ER+ Metastatic Breast Cancer Xenograft
NUV - 422 IS SUPERIOR TO FULVESTRANT IN XENOGRAFT MODEL OF ER+ METASTATIC BREAST CANCER Page | 15 Tumor Volume
Slide 16: Deep Tumor Reductions in Enzalutamide-Resistant Prostate Model
Complete Re sponses 0% 0% 10% 40% DEEP TUMOR REDUCTIONS OBSERVED IN ENZALUTAMIDE - RESISTANT PATIENT - DERIVED XENOGRAFT PROSTATE MODEL Tumor Volume (Day 39) Page | 16
Slide 17: Drug-Drug Conjugate (DDC) Platform
Drug - Drug Conjugate (DDC) Platform DDC1 [PARP - AR] (mCRPC) 2H22 Nominate DDC DDC2 [PARP - ER] (Ovarian/Breast Cancers) DDC3 - undisclos ed DDC4 - undisclos ed
Slide 18: DDC Platform Is an Advance Beyond ADCs
THE DRUG - DRUG CONJUGATE (DDC) PLATFORM IS A REVOLUTIONARY ADVANCE BEYOND ADCs Page | 18 Antibody Drug Conjugate Drug - Drug Conjugate Drug - Drug Conjugates x Tissue - selective targeting improves therapeutic index vs. untargeted warhead x Oral x Binds intracellular and cell membrane targets x Hig
Slide 19: DDCs Designed to Bind Two Different Targets Simultaneously
DRUG - DRUG CONJUGATES ARE DESIGNED TO BIND TWO DIFFERENT TARGETS SIMULTANEOUSLY Drug Target X Page | 19 Drug Target Y Drug X Drug Y Drug Target X Drug Target Y Fuse Binding Domains Drug X Drug Y
Slide 20: NUV-1156: DDCs That Target AR and PARP
NUV - 1156: NUVATION BIO HAS CREATED DRUG - DRUG CONJUGATES THAT TARGET AR AND PARP P ARP Page | 20 AR L y n pa r za Xtan d i P ARP AR Fuse Binding Domains Lynparza Xtandi Two Separate Drugs / Two Separate Targets PARP Inhibitory Warhead AR Targeting Small Molecule
Slide 21: NUV-1156 Exploits Low AR Expression in Sites of PARP Toxicity
NUV - 1156: EXPLOITS LOW AR EXPRESSION IN KNOWN SITES OF PARP - RELATED TOXICITY (BONE MARROW AND GI TRACT) Bone Marrow Duo d en u m Small Intestines Colon T estis P r osta t e Epididymis Seminal Vesicle Fallopian Tube Breast Cervix, Uterine Endometrium Androgen Receptor Expression Level SCORE High
Slide 22: NUV-1156 DDC Potently Kills Resistant Prostate Cancers
NUV - 1156 DDC POTENTLY KILLS PROSTATE CANCERS RESISTANT TO CURRENT STANDARD OF CARE NU V - 1 15 6 O l ap a rib En za lu ta m ide Olaparib + Enzalutamide NUV - 1156 + Enzalutamide NUV - 1156 + DHT 10 1 0.6 0.4 0.2 0.0 20 30 22 R V1 IC 50 (uM) CELL P R OLIFER A TION IC 50 (nM) >30,000 7844 + 6152 NUV
Slide 23: Approved PARP Inhibitors: Efficacy in HR-Deficient vs HR-Proficient Tumors
CURRENT APPROVED PARP INHIBITORS HAVE HIGHER EFFICACY IN HR - DEFICIENT VS. HR - PROFICIENT TUMORS >$7B IN 2025 PROJECTED SALES HR - DEFICIENT (HRD) 1/3 OF TU MO R S HR - PROFICIENT (HRP) 2/3 OF TU MO R S 2000 0 4000 10000 8000 6000 IC 50 (nM) HR deficient HR proficient Prostate cancer TNBC TNBC TNB
Slide 24: NUV-1156 Kills Enzalutamide-Resistant Prostate Cancer Cells, Spares Healthy Gut Tissue
Page | 24 NUV - 1156 KILLS ENZALUTAMIDE - RESISTANT PROSTATE CANCER CELLS BUT SPARES HEALTHY GUT TISSUE IN VITRO 0 . 3 uM 0 5000 15000 10000 30000 IC50 (nM) NUV - 1156 Olaparib Enzalutamide 22RV1 PROSTATE CELLS (CANCER CELLS) IEC - 6 RAT GUT EPITHELIAL CELLS (HEALTHY TISSUE) APPROVED PARP INHIBITORS
Slide 25: Prostate Cancer: $15B Market Opportunity
~600K Men Annually Surgery & Radiation Androgen Deprivation Tx Combined Androgen Blockade Non - Metastatic CRPC 1L mCRPC R/R mCRPC Salvage Tx / Hospice ▪ Erectile Dysfu n ct i on ▪ Urinary and Fecal Incontinence ▪ Invasive Surgical Risk THE ONLY POTENTIALLY CURATIVE PROCEDURE FOR PROSTATE CANCER IS
Slide 26: Vision: Pharmacological Prostatectomy
▪ NUV - 1156 has the potential to kill prostate cancer with unprecedented specificity, sparing blood vessels and nerve cells ▪ Potentially allows men to avoid surgical prostatectomy/radiation ablation VISION: USE PROSTATE SPECIFIC DDC TO ACHIEVE A NERVE/BLOOD VESSEL - SPARING “PHARMACOLOGICAL PROSTA
Slide 27: ER Expression Limited to Female Sex Organs
ER PROTEIN EXPRESSION IS LIMITED TO FEMALE SEX ORGANS; LOW EXPRESSION IN SITES OF PARP - RELATED TOXICITY Bone Marrow Duodenum Small Intestines Colon Smooth Muscle Fallopian Tube Breast Vagina Cervix, Uterine Endometrium Estrogen Receptor Expression Level SCORE High Me di um L o w N o t De t ec t ed
Slide 28: NUV-1176, ER-Targeted DDC, Kills HR-D and HR-P ER+ Breast Cancers
NUV - 1176, AN ER - TARGETED DDC, POTENTLY KILLS BOTH HR - D AND HR - P ER+ BREAST CANCERS WITHOUT KILLING HEALTHY GUT TISSUE IEC6 0 . 3 uM ER+ TUMOR CELL LINES H EA L T H Y TISSUE ER+ Breast cancer ER+, HER2+ Breast cancer ER+ Breast cancer ER+ Breast cancer N UV - 1 17 6 HR Deficient Page | 28 HR
Slide 29: NUV-868 | BET AML
NUV - 868 | BET AML 1H22 Initiate Ph1 Study
Slide 30: NUV-868 Is a More Selective BD2 Inhibitor
NUV - 868 IS A MORE SELECTIVE BD2 INHIBITOR BRD4 Affinity BD2 BD1 Selectivity NUV - 868 2 2920 1460x ABBV - 774 1.05 340 234x CPI - 0610 17 85 5x ABBV - 075 7 27 3.9x MK - 8628 17 26 1.5x INCB - 57643 59 81 1.4x BET inhibitors have historically targeted BD1 and BD2 non - selectively, causing GI toxi
Slide 31: NUV-868 Preclinical Anti-Tumor Activity in AML Models
▪ NUV - 868 demonstrates striking anti - tumor activity in two AML xenograft models NUV - 868 PRECLINICAL ANTI - TUMOR ACTIVITY IN AML MODELS MV - 4 - 11 Kasumi - 1 0 6 0 0 12 0 0 18 0 0 24 0 0 Tumor size (mm 3 ) 0 3 6 9 1 2 1 5 1 8 2 1 Days V e h i c l e 10 mg/kg 20 mg/kg 5 mg/kg 0 Page | 31 2 5 0
Slide 32: BD2 Selectivity Avoids Gut Toxicity of Historical BET Inhibitors
Page | 32 BD2 SELECTIVITY AVOIDS THE GUT TOXICITY OBSERVED WITH HISTORICAL BET INHIBITORS NUV - 868 (BD2 Selective) Avoids GI Toxicity ABBV - 075 (Dual BD1 / BD2) V ehi c le NUV - 868 30 mg/kg BID Treatment of mice for 10 days with BD 2 selective compound NUV - 868 shows no evidence of goblet cell l
Slide 33: NUV-868 Reverses Platelet Suppression in AML
Dose (mg/kg) RBC (10 6 /ul) PLT (10 3 /ul) NEUT (10 3 /ul) LYM (10 3 /ul) RET (10 9 /L) Vehicle - 10.4 842 0.20 7.45 361 NUV - 868 5 9.6 893 0.19 3.98 438 NUV - 868 10 10.2 1290 0.15 5.53 463 NUV - 868 20 10.2 1460 0.07 5.93 505 Page | 33 MV 4 - 11 AML Xenograft Hematology Panel 24 - hours post fina
Slide 34: NUV-569 | Wee1 Pancreatic Cancer
NUV - 569 | W ee1 Pancreatic Cancer 3Q22 Initiate Ph1
Slide 35: Wee1 Inhibitor Overview
Wee1 INHIBITOR OVERVIEW Tumors Activate Their Wee1 Checkpoint Page | 35 Arrest Their Own Replication Giving Them Time to Fix Their Damaged DNA Then Turn Off Their Own Wee1 TUMOR GROWTH Wee1 Inh i b it or TUMOR DEATH r a d iatio n replicate bad DNA Wee1 inhibitors force tumors to replicate damaged DN
Slide 36: Promise of Existing Wee1 Inhibitors Limited by Safety
Page | 36 Pancreatic Cancer (3) • Combo with gemcitabine • Phase 2 (n): 34 • Median OS of 21.7 months (4) Uterine Serous Carcinoma (2) • Monotherapy • Phase 2 (n): 27 (21 evaluable) • ORR: 30% Ovarian Cancer (1) • Combo with carboplatin • Phase 2 (n): 24 (21 evaluable) • ORR: 43% PROMISE OF EXISTING
Slide 37: NUV-569 – Highly Potent and Selective = Less Toxicity
NUV - 569 – HIGHLY POTENT AND SELECTIVE = LESS TOXICITY Page | 37 Compound Wee1 PLK1 IEC6 NUV - 569 7 687 2362 AZD1775 4 15 251 IC 50 (nM) ▪ PLK1 is a ubiquitous cell kinase that may be responsible for gut and bone marrow toxicity ▪ NUV - 569 is highly potent against Wee1 but avoids PLK1 unlike AZD1
Slide 38: NUV-569 Increases In Vitro Killing of Pancreatic Cancer Cells
▪ NUV - 569 shows strong synergy with standard - of - care gemcitabine and radiation ▪ In - vivo xenograft tumor models ongoing NUV - 569 INCREASES IN VITRO KILLING OF PANCREATIC CANCER CELLS BY CHEMO AND/OR RADIATION 0% 40% 30% 20% 10% 50% 60% 70% 80% 90% 100% % C e l l K i l l i n g NUV - 569 + Ge
Slide 39: Upcoming Catalysts
UPCOMING CATALYSTS C O N F I D E N T I A L 1H21 2H21 1H22 2H22 1H23 Dose First Patient in Ph1 GBM Study Initiate Ph1 in Metastatic Brain Tumors Initiate Ph1 in ER+ mBC Initiate Ph 1 in mCRPC Present PFS Data from Ph1 GBM Study CDK2/4/6 B E T W ee 1 A2 A Submit IND Initiate Ph1 in Acute Myeloid Leuke
Slide 40: Summary
Page | 40 • Broad and validated wholly - owned pipeline with strong IP protection o Up to 6 INDs in 6 years • Multiple drug lead candidates addressing large markets with blockbuster drug sales potential • Leveraging and improving upon validated drug mechanisms • Focused on best - in - class profiles
Slide 41: Transaction Summary
Transaction Summary
Slide 42: Transaction Summary
Page | 42 ▪ Business Combination and concurrent equity financings announced October 21, 2020 ▪ Transaction closing expected in 1Q 2021 TRANSACTION SUMMARY T r a n s a c t i o n S t r u c t u r e More than $850M pro forma cash (1)(2) $500M equity financings concurrent with the business combination, i
Slide 43: Pro Forma Equity Ownership, Sources and Uses
27% 22% 8% 42% PRO FORMA EQUITY OWNERSHIP ($M, EXCEPT SHARE AND PER SHARE DATA) Sources Panacea Trust Equity (1) $144 Estimated Cash Contributed from Balance Sheet (2) 239 Proceeds from Concurrent Equity Financings 500 Equity Consideration to Existing Nuvation Shareholders 1 , 5 00 Total Sources $ 2
Slide 44: Nuvation Bio + Panacea: Strong Strategic Rationale
▪ Proven Management Team ▪ Best - in - class Therapies ▪ Multiple Avenues for Growth ▪ Strong Balance Sheet STRONG INSTITUTIONAL INVESTOR SUPPORT NUVATION BIO + PANACEA: STRONG STRATEGIC RATIONALE $144M in trust + equity financing STRONG INSTITUTIONAL INVESTOR SUPPORT Page | 44
Slide 45: Panacea Management's Proven Track Record
PANACEA MANAGEMENT’S PROVEN TRACK RECORD L E A D E R S H I P T E A M B O A R D O F D I R E C T O R S OLEG NODELMAN Chief Executive Officer SCOTT PERLEN Chief Financial Officer SCOTT PLATSHON Chief Operating Officer CAROLINE STOUT Chief Investment Officer DAN BRADBURY Co - Founder and Chairman, Equil
Slide 46: History of Picking Winners
Page | 46 HISTORY OF PICKING WINNERS 400 300 200 100 0 500 700 600 800 900 1,000% Ma r - 13 J a n - 14 No v - 14 S e p - 15 Jul - 16 Ma y - 17 Ma r - 18 J a n - 19 No v - 19 S e p - 20 Eco R 1 NBI S&P Note: Past performance is not necessarily indicative of future results. Source: Capital IQ and EcoR
Slide 47: Medivation: The Most Successful Biotech SPAC in History
Page | 47 0.00 25.00 50.00 75.00 (Pri ce) $100.00 December - 04 November - 08 October - 12 September - 16 MEDIVATION: THE MOST SUCCESSFUL BIOTECH SPAC IN HISTORY 12/17/04 – Merged with Orion Acq. Corp II at market cap of ~$3M ($0.39/sh (1) ) $14.3B Acquisition by Pfizer (1) Reverse split adjusted fo