WHWK
Published on 04/19/2026 at 11:48 pm EDT
Kathleen S. Keegan1; Shihe Hou1; Ashwini B. Pai1; Enrico Bellomo1; Erik Kratzer1; VictorPeykov1; Bryan Ball1; Yifeng Wang2; Yaohua Hu2; Xia Wang2; Zhuozhi Wang2; Siwei Nie2; Yunying Chen2; Jijie Gu2; David J. Lennon1; David Dornan1
1Whitehawk Therapeutics, Morristown, NJ, USA; 2WuXi Biologics, Shanghai, China
David Dornan, PhD
I have the following relevant financial relationships to disclose: Employee of Whitehawk Therapeutics
Stockholder in Whitehawk Therapeutics
Disclosure Information
CA125
MUC16
Non-shed
MUC16 ECD
MUC16 is a heavily glycosylated cell-surface protein that plays a key role in cancer
progression by facilitating tumor cell proliferation, invasion, and immune evasion1,2
CA125, the well-known cancer antigen and biomarker, is a proteolytic cleavage product of MUC16 that is shed into the blood stream. Non-shed MUC16 extracellular domain (ECD) remains on the tumor cell surface1,2
MUC16 SLC34A2 (NaPi2b)
PTK7 ERBB2 (HER2) FOLR1 (FRα) TACSTD2
VTCN1 (B7-H4)
CDH6 CLDN6
7.8
7.2
7.1
7
6.9
5.2
5.2
2.1
MUC16 Expression Relative to Other ADC Targets in OC4
MUC16
SLC34A2 (NaPi2b)
PTK7
ERBB2 (HER2)
FOLR1 (FRalpha)
9.1
TACSTD2 (TROP2)
VTCN1 (B7-H4)
(TROP2)
CDH6
CLDN6
0 2 4 6 8 10
Expression (log2[TPM+1])
MUC16 Expression in Cancer
MUC16 is highly expressed in multiple tumor types, including ovarian, endometrial, cervical, pancreatic, and lung cancers, and has relatively low expression in normal tissues1-3
In ovarian cancer (OC), MUC16 expression is 2- to >100-fold higher than that of clinically validated and emerging ADC targets4
Previous ADCs targeting MUC16 (DMUC4064A and DMUC5754A) demonstrated response rates of 14% to 42% in patients with high MUC16 expression5,6
- Higher MUC16 expression correlated with greater clinical activity5,6
Common TRAEs included fatigue, nausea, and peripheral neuropathy; grade ≥3
TRAEs included neutropenia, fatigue, and ocular toxicity5,6
However, since these ADCs bound shed CA125, higher dosing was required to overcome target-mediated drug disposition5-8
1. Zhang XY, et al. Clin Exp Med. 2024;24:101. 2. Chen X, et al. Front Immunol. 2024;15:1356913. 3. Wang AJ, et al. Front Pharmacol. 2022;13:1093666. 4. O'Malley M, et al. Presented at SGO Annual Meeting on Women's Cancer 2026; Poster 1544. 5. Liu J, et al. Gynecol Oncol. 2021;163:473-80.
6. Liu JF, et al. Ann Oncol. 2016;27:2124-30. 7. Chen Y, et al. Cancer Res. 2007;67:4924-32. 8. Zhang XY, et al. Clin Chim Acta. 2025;565:119981.
CPT116
TOP1i
inhibitor
Carbon
bridge
Cleavable
linker
Fc-effector attenuated
PEG masking
Intracellular triple peptide cleavage site
Proprietary TOP1i payload
Linker-Payload (CPT113)
Carbon bridge cysteine re-pairing
Optimized DAR6 configuration
Stability-enhancing hydrolysis
Bioconjugation
Antibody targeting membrane-bound ECD of MUC16 for improved tumor targeting
Attenuated Fc region
Targeting
HWK-016 mAb Binding
(MUC16 ECD Engineered SK-OV-3)
DMUC5457A mAb Binding
(MUC16 ECD Engineered SK-OV-3)
40,000
30,000
20,000
10,000
0
0.0001 0.01 1 100
(302 × ULN)
1,000
800
600
400
200
0
0.0001 0.01 1 100
(302 × ULN)
OVCAR-3 (OV, MUC16high)
SW1990 (PAAD, MUC16medium)
SK-OV-3 (OV, MUC16low)
5,000
4,000
MFI
3,000
2,000
2,000
2,000
1,500
MFI
1,000
500
2,000
1,500
MFI
1,000
500
0
0.0001 0.01 1 100
Antibody (nM)
10,000
0
0.0001 0.01 1 100
Antibody (nM)
10,000
0
0.0001 0.01 1 100
Antibody (nM)
10,000
HWK-016 binding is dependent on MUC16 expression
HWK-016
Isotype-CPT113
Cell Line
EC50 (nM)
Max MFI
EC50 (nM)
Max MFI
OVCAR-3 (MUC16high)
0.51
4200
NA
39
SW1990 (MUC16medium)
0.18
1708
NA
52
SK-OV-3 (MUC16low)
NA
172
NA
159
HWK-016 mAb Binding
SW1990
DMUC5754A mAb Binding
SW1990
HWK-016 mAb
SW1990
DMUC5754A mAb
SW1990
3-fold
22-fold
8,000 1,500
6,000
MFI
4,000
2,000
1,000
MFI
500
0
0.0001 0.01 1 100
Antibody (nM)
10,000
0
0.0001 0.01 1 100
Antibody (nM)
10,000
CA125
Concentration
HWK-016 mAb
EC50 (nM)
Fold Change
0 U/mL
0.22
N/A
10,623 U/mL (304 × ULN)
0.67
3.0
CA125
Concentration
DMUC5754A mAb EC50 (nM)
Fold Change
0 U/mL
0.56
N/A
10,623 U/mL (304 × ULN)
12.4
22.2
3-fold shift in EC50 for HWK-016 mAb binding vs 22-fold shift in EC50 for DMUC5754 mAb indicates minimal potential for high levels of CA125 to affect HWK-016 cell surface binding
Note: In patients with cancer, high CA125 is defined as 2 × ULN (>70 U/mL).
HWK-016 mAb Internalization
SW1990
DMUC5754A mAb Internalization
SW1990
HWK-016 mAb
SW1990
2.6-fold
8,000
6,000
MFI
4,000
2,000
0
0.01 0.1 1 10
Antibody (nM)
100
25,000
DMUC5754A mAb
SW1990
10-fold
20,000
MFI
15,000
10,000
5,000
0
0.01 0.1 1 10
Antibody (nM)
100
CA125
Concentration
HWK-016 mAb
EC50 (nM)
Fold Change
0 U/mL
0.34
N/A
10,623 U/mL (304 × ULN)
0.89
2.6
CA125
Concentration
DMUC5754A mAb EC50 (nM)
Fold Change
0 U/mL
1.6
N/A
10,623 U/mL (304 × ULN)
~15.8
10.1
2.6-fold shift in EC50for HWK-016 mAb internalization vs 10-fold shift in EC50for DMUC5754 mAb indicates minimal potential for high levels of CA125 to affect HWK-016-mediated cancer cell internalization
Note: In patients with cancer, high CA125 is defined as 2 × ULN (>70 U/mL).
20.5%
18.8%
26.6%
HWK-016
Isotype-CPT113
Untreated
48h
Average % area/nucleus is shown Blue: Hoescht; Green: γ-H2AX
γ-H2AX Activation by HWK-016 (% Area / Nucleus)
γH2AX
H2AX
Cleaved PARP
5 days post-treatment
30 β-Actin
20
10
0
Isotype-CPT113 HWK-016
*, p<0.05, paired t-test
HWK-016 Cell Viability
OVCAR-3
DMUC5754A-mAb-CPT113 Cell Viability
OVCAR-3
HWK-016 mAb
SW1990
DMUC5754A mAb
SW1990
2.5-fold
120
Cell Viability %
100
80
60
40
20
0
0.0001 0.01 1 100
Concentration (nM)
CA125
Concentration
HWK-016 mAb
EC50 (nM)
Fold Change
0 U/mL
1.86
N/A
10,623 U/mL (304× ULN)
4.57
2.5
2.5-fold shift in EC50for HWK-016 induced inhibition of cell viability vs 146-fold shift in EC50for DMUC5754-mAb-CPT113 indicates minimal potential for high levels of CA125 to affect HWK-016-mediated cancer cell killing
Note: In patients with cancer, high CA125 is defined as 2× ULN (>70 U/mL).
120
146-fold
Cell Viability %
100
80
60
40
20
0
0.0001 0.01 1 100
Concentration (nM)
CA125
Concentration
DMUC5754A-mAb-CPT113 EC50 (nM)
Fold Change
0 U/mL
0.02
N/A
10,623 U/mL (304× ULN)
2.93
146.5
HWK-016
MUC16positive OVCAR-3
HWK-016
MUC16negative Raji-Luc
HWK-016
3:1 Co-Culture OVCAR-3:Raji-Luc
Isotype-CPT113 HWK-016
OVCAR-3 Cell Viability (%)
120
100
80
60
40
20
0
0.01 0.1 1 10 100
Concentration (nM)
120
Isotype-CPT113 HWK-016
Raji.luc Cell Viability (%)
100
80
60
40
20
0
0.01 0.1 1 10 100 1000
Concentration (nM)
120
Isotype-CPT113 HWK-016
Raji.luc Cell Viability (%)
100
80
60
40
20
0
0.01 0.1 1 10 100
Concentration (nM)
+
+
+ +
HWK-016
ADC
+
+
+
+
+
+
-
-
- -
-
-
-
- -
-
+
-
+
+
+
+
-
+
HWK-016
ADC
+
+
-
+
-
+ +
+
HWK-016 ADC
+
-
MUC16positive cell MUC16negative cell
HWK-016 Reduced Viability of MUC16negative Cells After Co-Culture with MUC16positive Cells Demonstrating Bystander Effect
HWK-016 Efficacy in OVCAR-3 (MUC16high)
HWK-016 Efficacy in CTG-3423 (MUC16high)
2,500
Tumor Volume (mm3)
2,000
1,500
1,000
DPBS
Isotype-CPT113 1 mg/kg
DMUC5754A 1 mg/kg
DMUC5754A-mAb-CPT113 1 mg/kg
HWK-016 1 mg/kg
750
Tumor Volume (mm3)
500
250
HWK-016 (6 mg/kg)
500
0
108% TGI;
4/7 CRs
0 7 14 21 28 35
0
0 7 14 21
103% TGI;
1/8 CR
28 35
Time (days) Time (days)
HWK-016 shows greater antitumor activity relative to DMUC5754A and DMUC5754A mAb conjugated to CPT113
Note: OVCAR-3 sheds large amounts of CA125 (>600 ULN)
HWK-016 In Vitro Plasma Stability
Dato-DXd In Vitro Plasma Stability1
Human plasma
Cynomolgus monkey plasma
Human plasma Monkey plasma Rat plasma Mouse plasma PBS + 1% BSA
10 10
8 8
% CPT116 Release
% Drug Release
6 6
4 4
2 2
0
0 5 10 15 20 25
CPT116 release in human and cyno plasma is minimal (≤0.4%)
Time (days)
0
0 7 14 21
Time (days)
1. Okajima D et al., Mol Cancer Ther. 2021 Dec;20(12):2329-2340.
Species
HNSTD
Findings
Cynomolgus monkey
60 mg/kg
(highest dose tested)
No mortalities, all findings consistent with TOP1i
payload class of ADC
HWK-016 60 mg/kg
HWK-016
CPT116
HWK-016 T1/2 consistent with highly
stable ADC (~10-13 days)
Very low levels of CPT116 payload (<0.01%) released from HWK-016 into circulation
Mean Concentration (ng/mL)
1,000,000
100,000
10,000
10
1
0.1
0.01
0 200 400
Time (hrs)
HWK-016 is a promising next generation MUC16-targeting ADC that leverages novel bioconjugation and linker-payload technologies to minimize off-target effects and increase the therapeutic index
HWK-016 selectively binds to the non-shed, ECD of MUC16 to ensure delivery to the tumor instead
of circulating CA125
HWK-016 demonstrated potent binding, internalization, and reduced cancer cell viability that are minimally impacted by addition of high levels of exogenous CA125
HWK-016 has bystander activity and robust anti-tumor activity in models of ovarian cancer with
tumor regressions observed at doses as low as 1 mg/kg
In a repeat dose toxicology study, HWK-016 was well tolerated with an HNSTD of 60 mg/kg, the highest dose tested, and minimal levels of released payload were observed
HWK-016 is currently being evaluated in a phase 1 study of patients living with advanced ovarian
and endometrial cancers (NCT07470853)
Disclaimer
Whitehawk Therapeutics Inc. published this content on April 19, 2026, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on April 20, 2026 at 03:47 UTC.