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Item 8.01. Other Events
On July 12, 2022, Leap Therapeutics, Inc. (the “Company”) will host a virtual research and development day (the “R&D Day”). The program will include presentations by members of Leap’s leadership team as well external thought leaders in Leap’s core development areas. Also on July 12, 2022, the Company issued a press release entitled “Leap Therapeutics Announces Initiation of New DKN-01 Clinical Trials in Gastric Cancer, Colorectal Cancer and Endometrial Cancer.” A copy of the corporate presentation for the R&D Day and the full text of the press release are filed as Exhibits 99.1 and 99.2, respectively, to this Current Report on Form 8-K and incorporated herein by reference; provided, however that information on or connected to our website referenced in the Company’s press release is expressly not incorporated by reference into or intended to be filed as a part of this Current Report on Form 8-K.
| Item 9.01. | Financial Statements and Exhibits. |
(d) Exhibits.
| Exhibit Number |
Description | |
| 99.1 | Leap Corporate Presentation | |
| 99.2 | Press release dated July 12, 2022 | |
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document). |
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SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| LEAP THERAPEUTICS, INC. | ||
| Dated: July 12, 2022 | By: | /s/ Douglas E. Onsi |
| Name: | Douglas E. Onsi | |
| Title: | Chief Executive Officer and President | |
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Exhibit 99.1
company presentation LEAP THERAPEUTICS DKN - 01 R&D Day July 12, 2022
Forward looking statements 2 This presentation contains forward - looking statements that involve substantial risks and uncertainties. All statements, other than statements of historical facts, contained in this presentation, including statements regarding our strategy, future operations, clinical trials, collaborations and partnerships, future financial position, future revenues, projected costs, prospects, plans and objectives of management, are forward - looking statements within the meaning of U.S. securities laws. The words “anticipate,” “believe,” “estimate,” “expect,” “intend,” “may,” “plan,” “predict,” “project,” “target,” “potential,” “will,” “would,” “could,” “should,” “continue,” and similar expressions are intended to identify forward - looking statements, although not all forward - looking statements contain these identifying words. Forward - looking statements are neither historical facts nor assurances of future performance. Instead, they are based only on our current beliefs, expectations and assumptions regarding the future of our business, future plans and strategies, projections, anticipated events and trends, the economy and other future conditions. Because forward - looking statements relate to the future, they are subject to inherent uncertainties, risks and changes in circumstances that are difficult to predict and many of which are outside of our control. We may not actually achieve the plans, intentions or expectations disclosed in our forward - looking statements, and you should not place undue reliance on our forward - looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward - looking statements we make. These and other risk factors are listed from time to time in reports filed with the Securities and Exchange Commission, including, but not limited to, our Annual Reports on Form 10 - K and our Quarterly Reports on Form 10 - Q. We assume no obligation to update any forward - looking statements, except as required by applicable law. This presentation does not constitute an offer to sell, or the solicitation of an offer to buy, any securities.
Agenda 3 DKK1 Biology and DKN - 01 Mechanism of action Colorectal cancer: Zev Wainberg , MD UCLA Prostate cancer: David Wise, MD, PhD New York University Gastric cancer : Samuel Klempner , MD Massachusetts General Hospital Endometrial cancer: Rebecca Arend , MD University of Alabama at Birmingham
DKN - 01 Overview 4 Important milestones in 2022 and 2023 Single agent activity in three indications Biomarker - targeted development Combinations with checkpoint inhibitors and chemotherapy Strategic partnership with BeiGene T C Cancer cell DKN - 01 DKK1
The role of DKK1 in cancer 5 Cance r cell DKK1 is produced and secreted by cancer cells, functions on several tumor pathways and nearby immune cells DKK1 V E GFR2 CKAP4 Angiogenesis A kt β - ca t enin DKK1 DKK1 PI3K Cance r cell T umor Cancer cells Myeloid - derived suppressor cell WNT F ZD LRP 5/6 Cell proliferation Blocks Wnt signaling, signals through CKAP4 and PI3K to activate Akt Angiogenesis Upregulates V E GFR2, inc r eases formation of tumor blood vessels Enhances MDS C cells Inhibits β - catenin dependent Wnt signaling to enhance suppressive activity Supp r esses NK cells Hel p s tumor cells escape NK cells
DKN - 01 - an anti - DKK1 antibody 6 Tumor Cancer cell DKN - 01 Single agent and combination activity demonstrated in three different tumor types. Well - tolerated as monotherapy and in combination with chemotherapy or checkpoint inhibitors. Reduces cell proliferation Blocks signaling through CKAP4 and PI3K to downregulate a kt Reduces angiogenesis Reduces blood vessel formation, upregulates key cytokines, IFNy, IL - 15 and IL - 33 Suppresses MDSC cells B - catenin dependent Wnt signaling reprograms MDSCs and reduces immunosuppressive activity DKN - 01 binds and removes free DKK1 from the TME: Activates NK cells Upregulates NK cell ligands on tumor, production of Granzyme B by activated NK cells
DKN - 01 + anti - PD - 1 combination 7 Enhances tumor microenvironment for immune cells to target and clear the tumor Activates CD8 T cells Stimulates activity of NK cells Induces pro - inflammatory tumor microenvironment Upregulates PD - L1 (the target for anti - PD - 1 antibodies) Anti - PD - 1 stimulates CD8 T cell adaptive immunity: DKN - 01 stimulates innate immune system:
Pipeline 8 DKN - 01 + anti - PD - 1 pembrolizumab DKN - 01 + docetaxel DKN - 01 DKN - 01 + anti - PD - 1 tislelizumab + chemotherapy (1L) DKN - 01 + anti - PD - 1 tislelizumab (2L) 1L PFS d ata, 2L initial data Q1 2022 Final 1L data expected in Q3 2022 1L Randomized Controlled Trial FPI Q4 2022 Investigator - initiated study Initial data Q2 2022 FPI Q3 2022 Investigator - initiated study Gastric/GEJ cancer Endometrial cancer Lung cancer Prostate cancer DKN - 01 + bevacizumab + chemotherapy Colorectal cancer FPI Q4 2022
DKN - 01 Gastric cancer development
DKK1 - high levels are associated with poor survival 10 Strata 21 34 7 1 1 20 4 0 300 200 100 0 time to treatment discontinuation (days) High l evels of DKK1 c orrelate with s horter o verall s urvival In g astric c ancer TCGA STAD d ataset DKK1 - high i s a ssociated with p oor r esponse to first - line platinum + fluoropyrimidine based therapies in GEJ/ gastric cancer patients Collaboration with Tempus DKK1 expression data (TCGA): DKK1 - high patients ~2.5 years shorter OS in DKK1 - high patients P a n c r e a t ic E s o p h a ge al Head and neck TNBC G / G E J P r o st a t e Lung adeno L i v er Uterine C RC overall su r vi v al overall su r vi v al DKK1 expression (RNA - Seq normalized log2) 16 14 12 10 8 6 4 2 0 DKK1 - low patients DKK 1 - l o w DKK 1 - high Days 0 4000 3000 2000 1000 100 Probability of s urvival 5 0 0 25 75 DKK1 - h igh (n=175) DKK1 - l ow (n=175) p - val = 0.0164 (Mantel - Cox) 0.00 Survival probability 1.00 0.75 0.50 0.25 p = 0.31 overall survival overall survival DKK1 - high DKK1 - low Number at risk
DKK1 expression determined using RNAscope 11 * H - s core cut - off at 35 (equating to TPS 20) was identified for gastric cancer from our study of DKN - 01 + pembrolizumab 0 50 100 150 200 250 300 DKK 1 - l o w DKK 1 - high DKK1 - low p atient (H - score = 4) DKK1 - high p atient (H - score = 108) Chromogenic in situ hybridization RNAscope The biopsy sample is stained to identify DKK1 mRNA Pathologist determines histology score (H - s core), measuring DKK1 expression rather than protein itself H - s core = 35 * Each red dot is an individual mRNA for DKK1 Number of cells and intensity of staining is converted to H - s core
DKN - 01 single agent activity in heavily pretreated esophagogastric cancer patients 12 Baseline 4 - month scan On study 1 year, reduction - 33.9% failed prior anti - PD - L1 + IDOi Best overall response of 20 evaluable patients* Partial response 2 Stable disease 6 Progressive disease 12 *By Blinded Independent Central Review 2L+ EGC DKN - 01 2 monotherapy PRs Clinical benefit rate 40% Left adrenal met = 30.8 mm Left adrenal met = 11.0 mm
*DKK1 - high ≥ upper tertile (35) Clinical activity of DKN - 01 plus paclitaxel or anti - PD - 1 antibody 13 PD PD PD PD PD PD PD PD PD PD PD SD SD SD SD SD SD SD SD SD SD SD SD SD SD SD SD SD SD SD PD PD PD PD PD PD PD PD PD PD PR PR PR PR PR PR PR PR PR PR PR PR PR PD PD PD PD PD PD PD PD PD PD PD PD SD SD SD SD SD SD PD SD PR PR PR PR PR 50% - 50% - 100% 100% DKN - 01 + paclitaxel N=52 DKN - 01 + paclitaxel Patients treated Prior therapies N =52 60% Disease c o n t r ol r at e (DCR) 25% Overall r espons e r at e (ORR) 2 L - 8 L esophagogastric pts GEJ/GC ESCC E C A C PD - progressive disease PR - partial response SD - stable disease T umo r types: 0 260% ORR in 2L patients is ~47% Strong broad activity in esophagogastric cancer in heavily pretreated patients DKN - 01 + paclitaxel Patients treated PFS (months) N =15 12 . 7 73.3% OS (months) Disease c o n t r ol r at e (DCR) 46.7% Overall r espons e r at e (ORR) 4. 5 1 - 7 Maximum percent decrease - 100% 50% - 50% - 30% 100% 20% GEJ/GC Historical data DKN - 01 + pemb r o N=31 2L + GEJ/GC pts Total (n) location RE (n) PR (n) SD (n) PD (n) NE (n) Disease c o n t r ol r at e ( DCR) Overall r espons e r at e (ORR) 0 % Achieved improved ORR, PFS, and OS in DKK1 - high patients Identified H - score threshold for DKK1 high/low expression n=11 n=20 10 5 3 2 1 0 3 12 5 8 (80%) 3 (20%) 5 (50%) 0 (0%) DKK1 - high DKK 1 - l ow 1 5 PD - progressive disease PR - partial response SD - stable disease OS ( mo ) 7.3 4 PFS ( mo ) 5.1 1 .4
DisTinGuish study design: advanced GEJ/Gastric cancer Assess the safety and anti - tumor activity of DKN - 01 in combination with tislelizumab +/ - chemo therapy DKN - 01 + t islelizumab/XELOX DKN - 01 + t islelizumab Overall Response Rate Progression - Free Survival Duration of Response Overall Response Rate Progression - Free Survival Duration of Response Part A: Fi rs t - line: Part B: Second - line: N=25 N= 51 Safety Safety DKK1 all DKK1 - high PD - 1 Naï v e 14 1L GEJ/GC DKN - 01 + t islelizumab + chemotherapy
DisTinGuish Part A consort diagram 15 DKK1 - high: H - score ≥35; DKK1 - low: H - score <35 1L GEJ/GC DKN - 01 + t islelizumab + chemotherapy 25 patients enrolled in ITT DKK1 - low ( ITT) DKK1 unknown expression C ompleted at least a full cycle of therapy (mITT) 1 unable to complete a full cycle of therapy 4 3 9 9 10 12 DKK1 - high ( ITT) C ompleted at least a full cycle of therapy (mITT) C ompleted at least a full cycle of therapy (mITT) 2 unable to complete a full cycle of therapy Still on treatment 21 - day cycles: IV DKN - 01 300mg IV DKN - 01 300mg IV tislelizumab 200mg IV oxaliplatin 130mg/m 2 oral capecitabine 1000mg/m 2 twice daily Days: 15 21 1
Best overall response by DKK1 expression 16 68.2% ORR in the mITT p opulation (1 CR; 14 PR) * mITT population includes all patients who received > 1 dose of DKN - 01 As presented at ASCO GI 2022 mITT * population N=22 DKK1 - high N=10 DKK1 - low N=9 DKK1 - unknown N=3 CR - complete response 1 (4.5%) 0 1 (11.1%) 0 PR - p artial response 1 4 (6 3 . 6 %) 9 (90.0%) 4 ( 44 . 4 %) 1 (33.3%) S D - s table disease 6 (27.3%) 0 4 (44.4%) 2 (66.7%) PD - p rogressive disease 0 0 0 0 NE - non - evaluable 1 (4.5%) 1 (10.0%) 0 0 SD SD SD SD SD SD PR PR PR PR PR PR PR PR PR PR PR PR PR PR C R - 50% - 30% 0 Best % cha n ge in sum of diameters GEJ Gastric All 9 of the evaluable DKK1 - high patients had a partial response 1 PR went to curative surgery with pathological CR - 10 0 % 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy
Durable response by DKK1 expression 17 90 % ORR in DKK1 - high patients Best % cha n ge in sum of diameters Best Response Tumor Type GEJ GC DKK1 RNAscope H - score status High (≥35) Low (<35) Unknown Time since first dose (months) 2 3 4 5 9 12 14 PR - partial response SD - stable disease 10 6 7 8 11 13 0 1 CR - complete response % Change from baseline in sum of diameters 20 0 - 40 - 100 - 20 - 60 - 80 As presented at ASCO GI 2022 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy
PFS longer in DKK1 - high patients Median PFS all: 10.7 mo Median PFS for DKK1 - high: 11.9 mo Median PFS from Checkmate - 649 (nivolumab + chemo): 7.7 months Median 95% Cl High ≥35 11.9 1.12 12.0 Low <35 10.7 4.07 NA Unknown 8.38 1.31 NA Progression - free survival by DKK1 status (N=25) 12 High ≥35 9 Low <35 4 Unknown 11 8 8 7 6 5 3 5 3 Kaplan - Meier estimate 1 0.6 0 0.8 0.4 0.2 Progression free survival (months) 2 3 4 5 9 12 14 10 6 7 8 11 13 0 1 DKK1 RNAscope H - score status High (≥35) Low (<35) Unknown censored 9 8 9 9 9 9 7 6 4 3 3 3 3 3 3 3 1 1 1 0 4 2 1 2 1 1 6 18 As presented at ASCO GI 2022 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy
Overall survival not reached 19 Median 95% Cl High ≥35 NA 1.12 NA Low <35 NA 4.83 NA Unknown NA 1.31 NA Overall survival by DKK1 status (N=25) 12 High ≥35 9 Low <35 4 Unknown 11 9 6 7 5 7 Kaplan - Meier estimate 1 0.6 0 0.8 0.4 0.2 Overall survival (months) 2 3 4 5 9 12 14 10 6 7 8 11 13 0 1 DKK1 RNAscope H - score status High (≥35) Low (<35) Unknown censored 9 9 9 9 9 8 4 3 3 3 3 3 3 3 1 1 1 1 5 2 2 4 2 1 9 9 9 9 8 8 As presented at ASCO GI 2022 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy Median OS from Checkmate - 649 (nivolumab + chemo): 13.8 months
Best overall response by PD - L1 expression 20 79 % ORR in PD - L1 low patients Best % change in sum of diameters vCPS: visually - estimated combined positive score; PD - L1: programmed death - ligand 1 *Includes one pathologic CR As presented at ASCO GI 2022 CR - complete response 1 (50%) PR - p artial response 3 (75%) 0 6 (100%) 4 (57%) * 1 (100%) S D - s table disease 0 1 (50%) 0 3 (43%) 0 PD - p rogressive disease 0 0 0 0 0 NE - n on - evaluable 1 (25%) 0 0 0 0 DKK1 - low DKK 1 - high DKK 1 - high DKK 1 - l ow DKK 1 - unkno wn N=4 N=2 N=6 N=7 N=1 N=14 N=6 CP S ≥5 PD - L1 79% ORR 67% ORR CP S < 5 PD - L1 0 - 50% - 30% PR SD SD SD SD SD SD PR PR PR PR PR PR PR C R PR PR PR PR PR PR - 10 0 % 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy
DKK1 and PD - L1 expression are not correlated 21 This population had low overall PD - L1 expression 200 300 100 40 10 50 80 20 60 90 30 70 100 0 DKK1 expression (H - score) 0 - 300 PD - L1 expression (CPS) 0 - 100 DKK1 0 Spearman correlation r = 0.061 p - value (two - sides) = 0.804 CR - complete response (n=1) P R - partial response (n=14) SD - stable disease (n=4) NE (n=1) As presented at ASCO GI 2022 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy
DKN - 01 plus tislelizumab and chemotherapy safety profile 22 1L GEJ /GC DKN - 01 + t islelizumab + chemotherapy Preferred terms: Part A (N=25) No. Patients (%) TEAEs leading to death within 30 days of last dose 3 (12%) Any adverse event 25 (100%) Grade ≥ 3 events 14 (56%) DKN - 01 - related 5 (20%) Serious adverse events 10 (40%) DKN - 01 - related 2 (8%) Events leading to DKN - 01 discontinuation 3 (12%) DKN - 01 - related 1 (4%) Events leading to DKN - 01 dose reduction 1 (4%) Drug - related adverse events DKN - 01 - related 14 (56%) Tislelizumab - related 17 (68%) Capecitabine - related 24 (96%) Oxaliplatin - related 25 (100%) Regimen - related 25 (100%) Combination DKN - 01+ tislelizumab + capox was well tolerated with manageable toxicity Most common DKN - 01 - related adverse events were low grade (G1/2): Fatigue, nausea, diarrhoea, neutrophil count decreased , platelet count decreased No Grade 4 events TEAEs leading to death (Grade 5) within 30 days of last dose • Pulmonary embolism (1) assessed by the investigator as related to regimen • Aspiration pneumonia (1) and hepatic failure (1) both assessed as possibly related to disease progression 5 patients experienced six Grade ≥3 DKN - 01 - related adverse events: Diarrhoea (1), neutrophil count decreased (1), blood phosphorus decreased (2), pulmonary embolism (2)
DisTinGuish Part C randomized study 1L GEJ/GC DKN - 01 + t islelizumab + chemotherapy 23 DKN - 01 + tislelizumab + SOC chemotherapy (XELOX or mFOLFOX6) Tislelizumab + SOC chemotherapy (XELOX or mFOLFOX6) N=80 N=80 Stratification factors: • DKK1 expression (TPS ≥ 20% vs < 20%) • PD - L1 (CPS ≥5 vs < 5) Key eligibility criteria: • No prior therapy for unresectable locally advanced or metastatic gastric/GEJ adenocarcinoma • RECIST v1.1 measurable disease • Her2 negative N=160 1:1 Primary objective: PFS DKK1 - high Secondary objectives: – PFS all patients – OS, DKK1 - high and all – ORR , DKK1 - high and all
DKN - 01 highlights in gastric cancer 24 DKK1 is an important new therapeutic target in gastric cancer DKK1 - high is associated with aggressive biology, poor response to standard 5 - FU therapy, and shorter survival 56% ORR 10.7m PFS 90% ORR 11.9m PFS Response is correlated with DKK1 expression and independent of PD - L1 expression DKN - 01 + anti - PD - 1 tislelizumab + chemo therapy (1L) DKK1 - low DKK1 - high PD - L1 CPS <5 PD - L1 CPS <5 DKK1 DKK1 - high 79 % ORR 100 % ORR 68 % ORR 10.7m PFS Overall
DKN - 01 Colorectal cancer development
Rationale for targeting colorectal cancer DKK1 elevated in advanced CRC (Tempus) • CRC is characterized by hyperactivation of the Wnt pathway, often believed to be the initiating and driving event • DKK1 drives resistance to 5FU; DKN - 01 has demonstrated prior synergy with 5FU - based regimen in GEA • Preclinically DKN - 01 treatment: • Shows additive activity with 5FU and is able to overcome 5FU - resistance in xenograft models • Has activity alone and with anti - PD - 1 in syngeneic models • Has activity in wild type and PIK3CA mutant models alone and with a PIK3CA inhibitor Stage 1+2 Stage 3+4 T - test, p = 3.9e - 10 DKK1 Expression log2(TPM+1) 9 6 3 0 12 26
DKN - 01 activity in combination with 5 - FU chemotherapy in colorectal cancer models 27 • DKN - 01 has efficacy in CRC syngeneic models including HCT116 • Additive activity was seen with 5FU chemotherapy • In a 5FU chemotherapy - resistant model, DKN - 01 demonstrates significant inhibition of tumor growth Data courtesy of Goel Lab at City of Hope Cancer Center Tumor volume (mm 3 ) HCT116 parental HCT116 5FU - resistant 2500 2000 1000 0 Days post - induction 15 13 11 9 7 5 3 1 150 100 50 0 Tumor volume (mm 3 ) Days post - induction 15 13 11 9 7 5 3 1 1500 500 Iso+DMSO DKN - 01+5FU DKN - 01+DMSO lso+5FU
DKN - 01 activity in combination with 5 - FU chemotherapy in colorectal cancer models 28 • DKN - 01 has efficacy in CRC syngeneic models including SW480 • Additive activity was seen with 5FU chemotherapy • In a 5FU chemotherapy - resistant model, DKN - 01 demonstrates significant inhibition of tumor growth Data courtesy of Goel Lab at City of Hope Cancer Center Tumor volume (mm 3 ) SW480 parental SW480 5FU - resistant 600 400 0 Days post - induction 15 13 11 9 7 5 3 1 200 100 50 0 Days post - induction 13 11 9 7 5 3 1 200 Iso+DMSO DKN - 01+5FU DKN - 01+DMSO lso+5FU 150 Tumor volume (mm 3 )
DKN - 01 activity in combination with PD - 1 antibody in colorectal cancer model 29 • DKN - 01 has efficacy in CRC syngeneic models including CT26 • Additive activity was seen with an anti - PD - 1 antibody Tumor size (mm 3 ) 2000 1000 0 Days (post - inoculation) 500 lgG2a mDKN - 01 + Anti - PD - 1 Anti - PD - 1 mDKN - 01 21 18 14 11 7 1500 Single Agent Activity Additive Activity with Anti - PD - 1 Antibody
DKN - 01 activity in combination with PI3 kinase inhibitor in colorectal cancer models 30 • DKN - 01 has efficacy in CRC xenograft models, including with PIK3CA mutation • Additive activity was seen with an PI3 kinase inhibitor HCT116 parental HCT116 + PIK3CA H1047R mutation 3000 2000 1000 0 1500 500 Tumor size (mm 3 ) 2000 1000 500 0 1500 Tumor size (mm 3 ) hulgG4 huDKN - 01 huDKN - 01 + BYL719 BYL719 Days (post - inoculation) 52 48 36 32 16 20 24 28 40 44 2500 Days (post - inoculation) 48 36 32 12 20 24 28 40 44 16
DKN - 01 colorectal cancer study 31 Randomized phase 2 study of FOLFIRI/FOLFOX and b evacizumab +/ - DKN - 01 as second - line treatment of advanced colorectal cancer 2L CRC DKN - 01 + bevacizumab + chemotherapy Primary objective: PFS (SOC: mPFS 5.7 mos ) Secondary objectives: – ORR (SOC: ORR 5%) – DoR – OS DKN - 01 + SOC chemotherapy (FOLFIRI or mFOLFOX6) + bevacizumab SOC chemotherapy (FOLFIRI or mFOLFOX6) + bevacizumab N=65 N=65 Stratification factors: • DKK1 expression Key eligibility criteria: • One prior 5 - FU based therapy for advanced colorectal adenocarcinoma • RECIST v1.1 measurable disease • MSS and absence of BRAFV600 mutation N=130 1:1 S a f e ty run in IA s a f e ty review DKN - 01 + SOC + bevacizumab N=20
DKN - 01 Endometrial cancer development
Endometrial Cancer 33 Most common gynecological cancer in the western world High DKK1 i s associated with poor response to anti - VEGF therapy in endometrioid endometrial cancer patients Anti - VEGF treatment: 81% 95% 69% 17% 20% 80% 60% 40% O v e r all Regional (70%) Localized (67%) Metastatic (9%) 100% 0 0.25 0.75 0.50 1.00 0 0 500 Continuance probability ~66,500 annual cases in the United States and the incidence is increasing Fourth most common cancer in women in the United States Clinical risk factors include estrogen - only hormone replacement, obesity, chronic anovulation, tamoxifen therapy, nulliparity, early menarche, and late menopause ~ 66,500 Source: American Cancer Society , Tempus real world evidence 5 - Year overall and relative survival: 16 11 1 5 9 8 1 3 0 1 1 1 Number at risk Strata: DKK1 - low DKK1 - high 4 00 3 00 2 00 1 00 Time to treatment discontinuation anti - VEGF (days)
Single agent activity in endometrial cancer 34 Single agent activity is very low, ranging from 3 - 20% 13% 6% 3% 9% 13.5% 14.3% 36% 63.5% 26% 20% 50% 25% pembrolizumab 1.8 0% mPFS (months) dostarlimab durvalumab lenvatinib everolimus bevacizumab avelumab Anti - PD(L) - 1: MSS/refractory PD - L1+ mTOR Anti - angiogenic 4.2 5.4 2.8 ORR DCR 7 5% 100 %
Eligible p a tie n ts • Recurrent EEC • Recurrent platinum - resistant /refractory EOC • Recurrent MMMT • ≥ 1 prior therapy • Measurable disease • 50% in each group with Wnt signaling alteration Phase 2 study design evaluating DKN - 01 monotherapy and in combination in advanced gynecologic malignancies 35 DKN - 01 300mg monotherapy E EC E EC E OC E OC MMMT MMMT N =29 N =24 N =14 N =19 N =9 N =16 N =59 Primary objective: Overall response rate (ORR) Secondary objectives: Exploring genetic mutations in the Wnt signaling pathway and tumoral DKK1 expression as predictive biomarkers N =5 2 EEC - epithelial endometrial cancer EOC - epithelial ovarian cancer MMMT - malignant mixed M ü llerian cancer DKN - 01 300mg + p aclitaxel 80 mg
Status Total CR PR SD PD NE ORR DCR DKK1 - high (≥18) * n=8 1 1 3 3 0 25% 63% DKK1 - low (<18) n=15 0 0 1 11 3 0% 7% Unknown n=6 0 0 5 1 0 0% 83% DKN - 01 monotherapy - overall response by DKK1 tumoral expression 36 CR PR SD SD PD PD PD PD PD PD PD PD PD PD PD PD PD SD SD SD — — PD PD SD SD SD SD — *H - score ≥ 18, upper tertile of overall study population DKK1 - high tumors have better ORR (25% vs. 0%) and clinical benefit (63% vs. 7%) Patients with unknown DKK1 expression include 3 patients with durable SD and Wnt activating mutations Overall response by DKK1 tumoral expression 100 0 - 100 200 Best % change from baseline in tumor size Subject PD - progressive disease SD - stable disease PR - partial response CR - complete response Durable clinical benefit in DKK1 - high tumors 222011 218010 207004 205004 206008 217005 208004 217003 206010 222012 222014 213002 201009 202001 218009 204011 213003 222013 201010 204008 207003 217002 218007 222010 201002 222002 223002 222001 203008 DKK1 - high patients have longer progression - free survival (4.3 vs. 1.8 months [HR 0.26; 95 CI: 0.09, 0.75]) 0 - 100 0 200 600 Time since first dose (days) 100 % change from baseline in tumor size DKK 1 - high DKK1 - low Unknown Response status: PD - progressive disease SD - stable disease PR - partial response CR - complete response 4 00 2L+ E E C DKN - 01 + monotherapy
Complete response in endometrial cancer patient on DKN - 01 monotherapy 37 Maximum percent ecrease - 100% - 60% - 20% - 80% - 40% 0% 37.5 % 56 % tumor reduction CR Treatment: DKN - 01 monotherapy Patient: 60 yo female with recurrent endometrial cancer Prior treatment: radiation and chemotherapy poorly tolerated (neuropathy and thrombocytopenia) Baseline disease characteristics: MSI - H, TMB: 46.65 Genetics: ARID1A, PIK3CA; DKK1 - high Enrolled in July 2018 mo n ths: 30 Monotherapy CR tumor reduction 2 0 14 10 8 2L+ E E C DKN - 01 + monotherapy
Pembrolizumab + lenvatinib in second - line endometrial cancer 1 KEYNOTE - 775 data presented at SGO 2021 2 FDA Approves LENVIMA® ( lenvatinib ) plus KEYTRUDA® (pembrolizumab) Combination Treatment for Patients with Certain Types of Endometrial Carcinoma. https://www.eisai.com/news/2019/news201967.html 38 Population: n ORR CR PR SD mPFS Post platinum - based therapy, all - comers (dMMR + pMMR) 411 31.9 % 6.6 % 25.3 % 47.0 % 7.2 months Post platinum - based therapy pMMR 346 30.3 % 5.2 % 25.1 % 48.6 % 6 .6 months Len vima + Keytruda KN - 775 31% 100% 89% Grade ≥3 treatment - emergent AEs 1 Any grade treatment - emergent AEs 1 Lenvima discontinuation 1 Fatal adverse reactions 1 most common AE's with Lenvima + Keytruda treated patients: hypertension (64.0%), hypothyroidism (57.4%), diarrhea (54.2%), nausea (49.5%), decreased appetite (44.8%), vomiting (36.7%), weight decrease (34.0%), fatigue (33.0%), arthralgia (30.5%), proteinuria (28.8%), anemia (26.1%), constipation (25.9%), urinary tract infection (25.6%). Keytruda discontinuation 19% 1,2 : Most common A E 's leading to discontinuation of Keytruda: adrenal insufficiency, colitis, pancreatitis and muscular weakness (2% each). AE's leading to interruption of Keytruda (49%) 2 : fatigue (14%), diarrhea, and decreased appetite (6% each), rash (5%), renal impairment, vomiting, increased lipase, decreased weight (4% each), nausea, increased blood alkaline phosphatase, and skin ulcer (3% each), adrenal insufficiency, increased , amylase , hypocalcemia,hypomagnesemia, hyponatremia, peripheral edema, musculoskeletal pain, and syncope (2% each). AE's leading to reduction or interruption of Lenvima (88%) 2 : fatigue (32%), hypertension (26%), diarrhea (18%), nausea, palmar - plantar erythrodysesthesia, vomiting (13% each), decreased appetite (12%), musculoskeletal pain (11 %), stomatisis (9%), abdominal pain, herorrhades (7% each), renal impairment, decreased weight (6% each), rash, headache, increased lipase, and proteinuria (5% each). Including gastrointestinal disorders: cardiac disorders: 0.5%, general disorders: 1.5%, infections: 0.7 %, decreased appetite : 0.2%, neoplasms, nervous system, psychiatric, renal, reproductive, or respiratory disorders: 0.2% each. 6 %
DKN - 01 plus pembrolizumab endometrial cancer study 39 * Move to Stage II based on ORR in Stage I 2 - 3 L E E C DKN - 01 + pembrolizumab Key eligibility criteria: • > 18 years of age • P athology - confirmed advanced or recurrent endometrial carcinoma • Non - endometrioid histologies included with a Wnt activating mutation • No more than 2 prior chemotherapy regimens • No prior PD - 1 or PD - L1 therapy • No known dMMR or MSI - H tumors Primary objective: Objective response rate (ORR) Secondary objectives: Clinical benefit, PFS, OS, DOR Open - label, phase 2 trial, Bayesian optimal phase II design, Investigator - initiated study with pembrolizumab supplied by Merck. Pembrolizumab 200mg IV Day 1 DKN - 01 300mg IV Day 1 and 15 Cycle 21 days Pembrolizumab 200mg IV Day 1 DKN - 01 300mg IV Day 1 and 15 Cycle 21 days DKK1 - high DKK1 - l o w N=15 N=15 N=15 N=15 Stage I Stage II * Stage II * Stage I
DKN - 01 Prostate cancer development
DKK1 and DKN - 01 in prostate cancer 41 David Wise ASCO 2017 DKK1 expression is regulated by AR in CRPC tumor biopsies CIBERSORT analysis shows DKK1 expression associated with reduced inflammatory infiltrate DKN - 01 has efficacy in a PC3 SCID xenograft p< 0.0001 10 5 0 - 5 - 10 DKK1 mRNA expression (log2 FPKM) Active NK cells p< 0.005 0.02% 0.01% 0% p< 0.05 0.08% 0.04% 0% CD8+T cells p < 0.005 0.10% 0.05% 0% *P < 0.0001 1000 0 800 600 400 200 Quartile of DKK1 expression DKK1 quartile Quartile of DKK1 expression Days post treatment NE - NE+ CRPC Isotype DKN - 01 Inactive NK cells DKK1 low DKK1 high AR+ AR - AR+ AR - 1 2 3 4 1 2 3 4 1 2 3 4 12 20 24 28 16 8 4 0
Investigator - initiated study in advanced metastatic castration - resistant prostate cancer ( mCRPC ) 42 DKN - 01 delays prostate cancer growth in pre - clinical models in an NK - cell dependent manner. DKK1 is upregulated in prostate cancers with low Androgen Receptor (AR) expression. DKK1 AR P r og r essed on ≥1 AR signaling inhibitor N on - r andomi z ed Phase 1/2 DKN - 01 + docetaxel DKN - 01 monotherapy No prior taxane Prior taxane or taxane intolerant
DKK1 expression N=2 4 H - score 0 15 ( 58.3 %) H - score ≥1 10 ( 41.7 %) H - score ≥10 5 ( 20.8 %) H - score ≥35 3 ( 12.5 %) DKN - 01 + Doc e ta x el 300mg N/A N=4 600mg N/A N=3 300mg 75mg/m 2 N=3 600mg 75mg/m 2 N=3 Age 64.5 74 66 68 Adenocarcinoma , n (%) 4 (100%) 3 (100%) 3 (100%) 1 (33%) Neuroendocrine carcinoma, n (%) 0 0 0 2 (67%) Aggressive variant (AVPC), n (%) 1 (25%) 0 1 (25%) 3 (100%) APC mutation, n (%) 1 (25%) 1 (33%) 1 (33%) 0 CTNNB1 mutation, n (%) 0 2 (67%) 0 0 Investigator - initiated study in advanced metastatic castration - resistant prostate cancer ( mCRPC ) 43 Primary endpoint : of the phase 1 dose escalation cohorts was safety, characterized by dose - limiting toxicity (DLT). Secondary endpoints : of the study was to correlate anti - tumor activity, DKK1 expression (cutoff H - score ≥ 1), and clinical evidence of aggressive variant prostate cancer (AVPC). Safety data overview: Baseline characteristics: • No DKN - 01 related Grade ≥ 3 adverse events occurred in either cohort • No unexpected d ocetaxel - related Grade ≥ 3 AEs were observed DKK1 expression in 42% of samples tested: 2L+ mCRPC DKN - 01 + docetaxel
DKN - 01 activity in advanced mCRPC patients Monotherapy N= 7 Combination N= 6 PR - p artial response 0 5 ( 83.3 %) S D - s table disease 2 ( 28.6 %) 0 PD - p rogressive disease 3 (42.9%) 0 NE - non - evaluable 2 ( 28 . 6 %) * 1 (1 6.7 %) * 1 NE patient in each group had no measurable disease at baseline 2L+ mCRPC DKN - 01 + docetaxel Combination with docetaxel Monotherapy DKN - 01 600mg plus docetaxel DKN - 01 300mg plus docetaxel Unconfirmed Tx Ongoing A AVPC * 0 - 0.2 - 0.4 - 0.6 - 0.8 Best Overall Response A A A* * 0 0 90 2 3 DKK1 1.0 0.5 0.0 - 0.5 - 1.0 Best Overall Response n/a 0 n/a 10 5 DKK1 DKN - 01 600mg DKN - 01 300mg 44 All 5 evaluable DKN - 01 plus docetaxel patients had a RECIST partial response (3 confirmed, 2 unconfirmed) Confirmed responses in 2 of 3 patients with AVPC KEYNOTE - 365 (cohort B), pembrolizumab plus docetaxel: 23% confirmed ORR by RECIST in evaluable patients
DKN - 01 activity in combination with docetaxel PFS Best PSA Response Best PSA Response (%) 100 50 0 - 50 - 100 mPFS, 6.4 months 100 75 50 25 0 Months 0 2 4 6 8 10 rPFS (n=6) pts treated with DKN - 01 plus Docetaxel. rPFS (%) DKN - 01 600mg plus Docetaxel DKN - 01 300mg plus Docetaxel 45 2L+ mCRPC DKN - 01 + docetaxel All 6 DKN - 01 plus docetaxel patients have had a PSA50 response (6 th patient PSA50 response post - data cut) KEYNOTE - 365 (cohort B), pembrolizumab plus docetaxel: 34% PSA50 response Tx Ongoing
-0.75 -0.5 -0.25 0 0 65 130 195 260 % Change from Baseline Days on Treatment Confirmed partial response with deepening of response on monotherapy 46 Docetaxel plus DKN - 01 DKN - 01 Monotherapy * * Docetaxel discontinued due to toxicity Continued tumor regression with DKN - 01 treatment observed after discontinuation of docetaxel Treatment: DKN - 01 plus docetaxel transitioned to DKN - 01 monotherapy Patient: 6 9 yo male with metastatic castration resistant prostate cancer Prior treatment: Radical prostatectomy, pelvic RT, enzalutamide + 6 cycles of prostvac , bicalutamide, Lupron with immediate progression, darolutamide , sipuleucel - T with new liver lesions and biopsy proven prostate adenocarcinoma Biomarkers : NHTL1 mutation, DKK1 H - score = 0
DKN - 01 highlights in prostate cancer 47 Non - clinical studies identified DKK1 as being upregulated in prostate cancers with low Androgen Receptor expression and that inhibition of DKK1 delayed prostate cancer growth DKN - 01 in combination with docetaxel showed promising clinical responses in unselected patients by both RECIST and PSA50 criteria Clinical activity was particularly promising in patients with Aggressive Variant Prostate Cancer Retrospective correlation of anti - tumor activity with biomarker status is ongoing DKK1 AR
DKN - 01 DEVELOPMENT STRATEGY 2022 - 2023 Milestones
Leap 2022 - 2023 clinical milestones Prostate cancer + docetaxel Part A: First - line patients combination with chemotherapy Part B: Second - line patients DKK1 - high Part C: First - line patients Randomized Controlled Trial Gastric cancer + tislelizumab 49 Colorectal cancer + bevacizumab + chemotherapy Endometrial cancer + pembrolizumab Q 1 Q 1 Q2 Q2 Q3 2 0 2 2 2 0 2 3 Q3 Q 4 Q 4 PFS Final Data LPI Final Data FPI Initial Data Initial Data FPI Initial Data FPI Initial Data
QUESTIONS & ANSWERS
Exhibit 99.2
Leap Therapeutics Announces Initiation of New DKN-01 Clinical Trials
in Gastric Cancer, Colorectal Cancer and Endometrial Cancer
Randomized Controlled First-Line Gastric Cancer Trial of DKN-01 plus tislelizumab and chemotherapy
in collaboration with BeiGene
Leap to host R&D Day today at 12:00 p.m. ET
CAMBRIDGE, Mass., July 12, 2022 – Leap Therapeutics, Inc. (Nasdaq:LPTX), a biotechnology company focused on developing targeted and immuno-oncology therapeutics, and BeiGene, Ltd. (Nasdaq: BGNE; HKEX: 06160; SSE: 688235), a global, science-driven biotechnology company focused on developing innovative and affordable medicines to improve treatment outcomes and access for patients worldwide, today announced the initiation of Part C of the ongoing DisTinGuish study to evaluate DKN-01, Leap’s anti-Dickkopf 1 (DKK1) antibody, in combination with tislelizumab, BeiGene's anti-PD-1 antibody, and chemotherapy compared to a tislelizumab and chemotherapy control arm, in patients with gastric or gastroesophageal junction cancer (G/GEJ).
Additionally, Leap is initiating a new company-sponsored trial of DKN-01 in combination with standard of care bevacizumab and chemotherapy in second-line patients with colorectal cancer that is designed to expand into a randomized study. Leap is also supporting an investigator-initiated trial of DKN-01 plus pembrolizumab in patients with endometrial cancer to be conducted at The University of Texas M.D. Anderson Cancer Center and at the University of Alabama at Birmingham.
Leap’s management team, together with key opinion leaders, will host an R&D Day today to provide updates on the Company’s DKN-01 program including G/GEJ, colorectal cancer, endometrial cancer, and prostate cancer.
“Since the presentation of the data for DKN-01 plus tislelizumab and chemotherapy in first-line G/GEJ patients demonstrating compelling overall response rates and progression-free survival, Leap and BeiGene have been working together to create an optimal global strategy for this unique combination therapy. We are excited to enhance the development program and our collaboration with BeiGene through a randomized controlled trial in first-line patients, with a focus on those patients whose tumors express high levels of DKK1,” said Douglas E. Onsi, President and Chief Executive Officer of Leap.
“Based on our clinical and preclinical data, Leap is committed to developing DKN-01 aggressively in multiple indications,” said Cynthia Sirard, MD, Chief Medical Officer of Leap. “Through a strategic review and prioritization process, we have decided to initiate a company-sponsored study in second-line colorectal cancer patients of DKN-01 in combination with standard of care bevacizumab and chemotherapy. We will also support an investigator-initiated study in endometrial cancer patients of DKN-01 in combination with pembrolizumab, building on previous data showing single-agent activity of DKN-01.”
R&D Day:
Leap’s management team will host an R&D Day today at 12:00 p.m. Eastern Time and will be joined by key opinion leaders:
Samuel Klempner, MD, Associate Professor at Harvard and Massachusetts General Hospital;
Zev Wainberg, MD, Co-Director of the GI Oncology Program at University of California Los Angeles;
Rebecca Arend, MD, Assistant Professor at University of Alabama at Birmingham Comprehensive Cancer Center; and
David Wise, MD, PhD, Assistant Professor at NYU Langone Health.
The live webcast presentation of the R&D Day can be accessed by registering at https://edge.media-server.com/mmc/p/4zp7m6pw. A replay of the event will be available for a limited time and may be accessed on the Investors page of the Company's website at https://investors.leaptx.com/
Gastric Cancer
The DisTinGuish study (NCT04363801) is a Phase 2 study of DKN-01 in combination with tislelizumab and standard of care (SOC) chemotherapy in patients with inoperable, locally advanced, G/GEJ adenocarcinoma. Part C of the DisTinGuish study will enroll approximately 160 first-line, HER2-negative patients who have had no prior therapy for unresectable locally advanced or metastatic G/GEJ adenocarcinoma. Patients will be randomized 1:1 to study DKN-01 in combination with tislelizumab and SOC chemotherapy, compared to tislelizumab and SOC chemotherapy. The primary objective of Part C is progression-free survival (PFS) in patients whose tumors express high levels of DKK1 (DKK1-high). Secondary objectives of Part C include PFS in all patients regardless of DKK1 expression, as well as overall survival (OS) and objective response rate (ORR) as measured by RECIST v1.1 in DKK1-high and all patients.
Part A and Part B of the DisTinGuish study are currently being conducted in the United States and the Republic of Korea. Part A enrolled 25 first-line HER2- G/GEJ cancer patients. As of December 10, 2021, the median PFS for all patients in Part A was 10.7 months, with 11.9 months PFS for DKK1-high patients, and the ORR for all patients who had completed a full cycle of therapy was 68%, with 90% ORR for DKK1-high patients. Part B of the study has enrolled 51 patients with second-line DKK1-high G/GEJ cancer. Additional follow-up data from Part A is expected to be presented in the third quarter 2022 and from Part B in the fourth quarter 2022.
Colorectal Cancer
The DeFianCe study is a Phase 2 study of DKN-01 in combination with bevacizumab and SOC chemotherapy in patients with advanced colorectal cancer who have received one prior systemic therapy. The study is designed with an initial 20 patient cohort and to then expand into a 130 patient randomized controlled trial against bevacizumab and SOC chemotherapy. The primary objective is PFS. Secondary objectives include ORR, duration of response (DOR), and OS. The study is expected to enroll its first patient in the third quarter 2022.
Endometrial Cancer
The investigator-initiated trial of DKN-01 in combination with pembrolizumab is an open-label, Bayesian design, Phase 2 trial and will initially enroll 15 patients each into DKK1-high and DKK1-low cohorts. If the efficacy criteria is met in either or both of the 15 patient cohort(s), then the cohort(s) will be expanded by an additional 15 patients. The primary objective of the study is ORR. Secondary objectives include clinical benefit rate (CBR), PFS, OS, and DOR. The study is expected to enroll its first patient in the fourth quarter 2022.
Leap has previously studied DKN-01 as a monotherapy and in combination with paclitaxel in patients with endometrial cancer. In the group of 23 patients treated with DKN-01 monotherapy for whom DKK1 expression data was available, patients with DKK1-high tumors achieved 1 complete response and 1 partial response, along with greater ORR (25% vs. 0%), CBR (63% vs. 7%), and median PFS (4.3 months vs. 1.8 months [HR 0.26; 95 CI: 0.09, 0.75]) compared to patients with DKK1-low tumors. In the group of 24 patients treated with DKN-01 plus paclitaxel, 72% of whom had received three or more prior systemic therapies, DKK1-high patients had improved median PFS (5.4 months vs. 1.8 months [HR 0.34; 95% CI: 0.12, 0.97]) compared to DKK1-low patients.
About DKN-01
DKN-01 is a humanized monoclonal antibody that binds to and blocks the activity of the Dickkopf-1 (DKK1) protein. DKK1 modulates the Wnt/Beta-catenin and PI3kinase/AKT signaling pathways and has an important role in promoting tumor proliferation, metastasis, angiogenesis, and in mediating an immune suppressive tumor microenvironment through enhancing the activity of myeloid-derived suppressor cells and downregulating NK cell ligands on tumor cells. The U.S. Food and Drug Administration has granted DKN-01 Orphan Drug Designation for the treatment of gastric and gastroesophageal junction cancer and Fast Track Designation in combination with tislelizumab for the treatment of patients with gastric and gastroesophageal junction adenocarcinoma whose tumors express high DKK1 protein, following disease progression on or after prior fluoropyrimidine- and platinum- containing chemotherapy and if appropriate, human epidermal receptor growth factor (HER2)/neu-targeted therapy.
About the Leap/BeiGene Collaboration
Leap is conducting the DisTinGuish study as part of an exclusive option and license agreement with BeiGene for the development of DKN-01 in Asia (excluding Japan), Australia, and New Zealand. Leap retains exclusive rights for the development, manufacturing, and commercialization of DKN-01 for the rest of the world.
About Leap Therapeutics
Leap Therapeutics (Nasdaq: LPTX) is focused on developing targeted and immuno-oncology therapeutics. Leap's most advanced clinical candidate, DKN-01, is a humanized monoclonal antibody targeting the Dickkopf-1 (DKK1) protein. DKN-01 is being developed in patients with esophagogastric, gynecologic, colorectal, and prostate cancers. Leap has entered into a strategic collaboration with BeiGene, Ltd. for the rights to develop DKN-01 in Asia (excluding Japan), Australia, and New Zealand. For more information about Leap Therapeutics, visit http://www.leaptx.com or view our public filings with the SEC that are available via EDGAR at http://www.sec.gov or via https://investors.leaptx.com/.
FORWARD-LOOKING STATEMENTS
This press release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, Section 21E of the Securities Exchange Act of 1934, as amended, and the Private Securities Litigation Reform Act of 1995, which involve risks and uncertainties. These forward-looking statements include statements regarding Leap’s business strategies, collaborations and partnerships, and expectations with respect to the development and advancement of DKN-01 in clinical trials, including the outcomes, status and timing of current or future studies. Although Leap believes that the expectations reflected in such forward-looking statements are reasonable as of the date made, forward-looking statements are subject to known and unknown risks, uncertainties and other factors that could cause actual results to differ materially from our expectations. Such risks and uncertainties include, but are not limited to: the uncertain clinical development process, including the risk that clinical trials may not have an effective design or generate positive results; that the initiation, conduct, and completion of clinical trials, laboratory operations, manufacturing campaigns, and other studies may be delayed, adversely affected, or impacted by COVID-19 related issues; unstable global market and economic conditions; the accuracy of our estimates regarding expenses, future revenues, capital requirements and needs for financing; the benefits to be derived from our agreement with BeiGene, Ltd. (“BeiGene”) or any other collaborations, license agreements, or other acquisition efforts; the rate and degree of market acceptance of DKN-01; the success of other competing therapies that may become available; the manufacturing capacity for DKN-01; our ability to maintain and protect our intellectual property rights; and other risks and uncertainties. Detailed information regarding factors that may cause actual results to differ materially from expectations is included in Leap Therapeutics' periodic filings with the SEC, including Leap's Annual Report on Form 10-K for the fiscal year ended December 31, 2021, as filed with the SEC on March 11, 2022 and as may be updated by Leap's Quarterly Reports on Form 10-Q and the other reports Leap files from time to time with the SEC. Any forward-looking statement contained in this release speaks only as of its date. Leap undertakes no obligation to update any forward-looking statement contained in this release to reflect events or circumstances occurring after its date or to reflect the occurrence of unanticipated events.
CONTACT:
Douglas E. Onsi
President & Chief Executive Officer
Leap Therapeutics, Inc.
617-714-0360
donsi@leaptx.com
Matthew DeYoung
Investor Relations
Argot Partners
212-600-1902
leap@argotpartners.com