CONCLUSIONS

P043

Updated Efficacy and Safety of the Tetravalent Death

Receptor 5 Agonist INBRX-109 in Patients With Chondrosarcoma:

Data From the Phase 1 Expansion Cohorts

Sant P. Chawla, MD1; Anthony Paul Conley, MD2; Christopher Lieu, MD3; Breelyn A. Wilky, MD3; Anthony Tolcher, MD4; Joseph Chao, MD5; Nehal J. Lakhani, MD, PhD6; Maria Diab, MD7; David Berz, MD, PhD8; Lane Senne, MS9;

Brianne O'Neill, PhD9; Miranda Fox, BS9; Vasily Andrianov, MD9; Brendan Eckelman, PhD9; Robert G. Maki, MD, PhD10; Vivek Subbiah, MD2

1Sarcoma Oncology Research Center, Santa Monica, CA, USA; 2The University of Texas MD Anderson Cancer Center, Houston, TX, USA; 3University of Colorado, Aurora, CO, USA; 4NEXT Oncology, San Antonio, TX, USA; 5City of Hope, Duarte, CA, USA;

6START Midwest, Grand Rapids, MI, USA; 7Emory University, Atlanta, GA, USA; 8Valkyrie Clinical Trials, Los Angeles, CA, USA; 9Inhibrx, Inc, La Jolla, CA, USA; 10Abramson Cancer Center, Philadelphia, PA, USA

INTRODUCTION

• Unresectable or metastatic conventional chondrosarcoma has a poor

prognosis, with a progression-free survival (PFS) of <4 months1-3

- Chemotherapy and radiation are largely ineffective, and no standard

targeted therapies are available3,4

INBRX-109 Mechanism of Action

• INBRX-109 is a third-generation, tetravalent, agonistic antibody against DR5

precisely engineered for optimal agonism and safety (Figure 1)

- The valency of INBRX-109 was empirically selected to include 4 DR5-binding

domains to overcome the limitations of earlier-generation agonists and potently

Figure 1. Structure of INBRX-109

METHODS

  • INBRX-109phase 1 study (NCT03715933) is an open-label, multicenter, dose-escalation study (Figure 2)

Figure 2. Study Design

• Death receptor 5 (DR5) is a proapoptotic receptor that has long

been a target of interest in oncology, including sarcomas, due to

the greater sensitivity of tumor cells over healthy cells to

DR5-mediated apoptosis5,6

• DR5 is widely expressed on tumor cells and is activated upon binding to

the tumor necrosis factor-relatedapoptosis-inducing ligand (TRAIL)5,6

- The binding of trimeric TRAIL to 3 death receptors leads to receptor

clustering and induction of the extrinsic apoptosis pathway

- TRAIL selectively induces programmed cell death in cancer cells, with

minimal impact on normal tissues, and therefore plays an important role

in tumor and viral immune surveillance

- While the trimer is the minimal functional unit for TRAIL activity,

agonize DR5 through efficient receptor clustering

- Immunogenic epitopes were removed to prevent antidrug antibody-mediated

cross-linking, lessening the potential for hyperclustering and concomitant

hepatotoxicity observed with previous multivalent DR5 agonists

• INBRX-109 is based on a single-domain antibody platform

- It consists of 2 identical camelid heavy-chain-onlyantigen-binding domains

targeting DR5 joined end to end with an effector-silenced Fc constant domain

based on human immunoglobulin G1

• The safety and tolerability of INBRX-109 monotherapy were demonstrated in

patients with diverse solid tumors during part 1 of an ongoing phase 1 study

(NCT03715933)

DR5: sdAb

DR5: sdAb

DR5: sdAb

DR5: sdAb

Fc: effector function disabled

106 kDa

Eligibility Criteria

Part 1: 3+3 Dose Escalation

• Metastatic or unresectable solid tumors refractory

•

All-comers 3+3 design evaluating doses of

to or intolerant of standard therapy or for which no

0.3 to 30 mg/kg

standard therapy exists

• INBRX-109 was well tolerated; MTD was

• Patients with chondrosarcoma

not reached

- Cohort A4: any tumor type or grade

•

Part 1 is now complete

- Cohort B4: all chondrosarcoma subtypes

and histological grades

- Cohort B6: only conventional, histological grade 2

A5

30 mg/kg

or 3, IDH1 (R132) or IDH2 (R172) mutation

A4

10 mg/kga

• No prior exposure to DR5 agonists

A3

3 mg/kg

A2

1 mg/kg

• Exclusion of chronic liver diseases; evidence or history

A1

0.3 mg/kg

of HBV, HCV, or HIV infection; or acute viral or toxic

liver disease within 4 weeks prior to the first dose

MTD and RP2D

of study drug

3 mg/kg selected as RP2D

Primary endpoint: safety and tolerability of INBRX -109

Exploratory endpoint: assessment of antitumor activity by Response Evaluation Criteria in Solid Tumors v1.1

B1

B2

B3

B4

B5

B6

B7

B8

C1

C2

C3

C4

C5

Part 2: Single-Agent Expansionb

Colorectal adenocarcinoma (n=20)

Gastric adenocarcinoma (n=10)

Malignant pleural mesothelioma (n=20)

Chondrosarcoma (n=20)

Synovial sarcoma (n=10)

IDH1/IDH2-mutant conventional chondrosarcoma (n=12)

Nonconventional chondrosarcoma (n=12)

Solid tumors, BMI >30 (n=12)

Part 3: Combination Therapy Expansion

Mesothelioma with carboplatin or cisplatin (n=10); carboplatin or cisplatin and pemetrexed (n=10)

Pancreatic adenocarcinoma 2L with mFOLFIRI (n=20)

Ewing sarcoma 2L-4L with irinotecan and temozolomide (n=20)

Colorectal adenocarcinoma with FOLFIRI (n=20)

SDH-deficient GIST or solid tumors with temozolomide (n=20)

clustering of multiple receptors at the cell-cell interface results in

maximal apoptotic activity7-9

• We provide updated results for patients with unresectable or metastatic

chondrosarcoma in this trial

DR5, death receptor 5; sdAb, single-domain antibody.

2L, second line; 4L, fourth line; BMI, body mass index; DR5, death receptor 5; FOLFIRI, fluorouracil, leucovorin, and irinotecan; GIST, gastrointestinal stromal tumor; HBV, hepatitis B virus; HCV, hepatitis C virus; IDH, isocitrate dehydrogenase; mFOLFIRI, modified FOLFIRI (fluorouracil and irinotecan); MTD, maximum tolerated dose; RP2D, recommended phase 2 dose; SDH, succinate dehydrogenase.

  1. Analysis includes 1 patient from dose-escalation cohort A4 (INBRX-109 10 mg/kg); b Based on historic data with prior DR5 agonists, preclinical in-house sensitivity screens, and literature. Planned enrollment is shown.

RESULTS

Patients

  • A total of 33 patients with chondrosarcoma were included in the analysis
    (data cutoff: May 26, 2022) (Table 1)
    • Patients were from cohorts A4 (any tumor, including chondrosarcoma; n=1), B4 (any chondrosarcoma subtype; n=22), and B6 (isocitrate dehydrogenase 1/2 [IDH1/IDH2]-mutant conventional chondrosarcoma; n=10)
  • As of the cutoff date, 9 of 33 patients continued receiving study treatment

Table 1. Baseline Demographics and Patient Characteristics

Chondrosarcoma,

IDHmt conventional

Total

Category

anya

chondrosarcomab

(n=23)

(n=10)

(n=33)

Age, years

Mean (SD)

57.6 (16.7)

50.9 (14.8)

55.6 (16.24)

Male, n (%)

18 (78.3)

8 (80.0)

26 (78.8)

Cancer stage, n (%)

I-II

1

(4.3)

0

1

(3.0)

III-IV

18 (78.3)

8 (80.0)

26 (78.8)

Unknown

4

(17.4)

2 (20.0)

6

(18.2)

IDH1/IDH2 mutation status, n (%)

IDH1

1

(4.3)

9 (90.0)

10 (30.3)

IDH2

0

1 (10.0)

1

(3.0)

No or unknown

22 (95.7)

0

22 (66.7)

Histological grade, n (%)c

n=16

n=10

n=26

Grade 2

9

(56.3)

8 (80.0)

17 (65.4)

Grade 2/3

2

(12.5)

2 (20.0)

4

(15.4)

Grade 3

5

(31.3)

0

5

(19.2)

Prior anticancer surgery, n (%)

22 (95.7)

10 (100.0)

32 (97.0)

Prior anticancer radiation, n (%)

8

(34.8)

4 (40.0)

12 (36.4)

Lines of prior systemic therapy,

1.0 (0-12)

1.5 (0-4)

1.0 (0-12)

median (range), n

Prior systemic therapy, n (%)d

Chemotherapy

10 (43.5)

4 (40.0)

14 (42.4)

Immunotherapy

8

(34.8)

5 (50.0)

13 (39.4)

Molecularly targeted therapy

4

(17.4)

6 (60.0)

10 (30.3)

Biologicse

2

(8.7)

0

2

(6.1)

None

7

(30.4)

1 (10.0)

8

(24.2)

IDHmt, isocitrate dehydrogenase 1/2 mutant.

  1. Includes 1 patient from dose-escalation cohort A4 (INBRX-109 10 mg/kg) and 22 patients from dose-expansion cohort B4 (INBRX-109 3 mg/kg). Two patients did not have conventional chondrosarcoma but were included because this was not an exclusion criterion at the time of their enrollment; b Two patients were excluded from the analysis due to taking prohibited medication (n=1) and having dedifferentiated chondrosarcoma (n=1); c Histological grade was determined using pathology reports reviewed on an individual patient basis. Only evaluable patients and those with conventional chondrosarcoma were included; d Patients could have received >1 systemic therapy; e Biologics included ozuriftamab vedotin (BA3021) and DeltaRex-G (n=1 for each).

Safety

Table 2. Treatment-Related AEs Reported in >5% of Patients

Chondrosarcoma (n=35)a

Preferred term, n (%)

Any grade

Grade ≥3

≥1 Treatment-related AE

(20.0)

2 (5.7)

7

Alanine aminotransferase increased

4

(11.4)

0

Aspartate aminotransferase increased

3

(8.6)

0

Blood bilirubin increased

2

(5.7)

1 (2.9)

Fatigue

2

(5.7)

0

Nausea

1

(2.9)

0

Blood alkaline phosphate increased

1

(2.9)

0

AEs were recorded using MedDRA preferred terms and graded according to CTCAE v5.0. Related AEs are those considered to be possibly, probably, or likely/certain to be related to INBRX-109 by the principal investigator. AE, adverse event; CTCAE, Common Terminology Criteria for Adverse Events; IDH, isocitrate dehydrogenase; MedDRA, Medical Dictionary for Regulatory Activities. a Includes 1 patient from dose-escalation cohort A4 (INBRX-109 10 mg/kg), 22 patients from dose-expansion cohort B4 (INBRX-109 3 mg/kg), and 12 patients from dose-expansion cohort B6 (IDH1/IDH2-mutant chondrosarcoma; INBRX-109 3 mg/kg).

  • The most common (>5% of patients) treatment-related adverse events (AEs) in patients with chondrosarcoma were increased alanine aminotransferase, increased aspartate aminotransferase, increased blood bilirubin, and fatigue (Table 2)
  • Among patients with frequent treatment-related AEs, no grade 4 or 5 events were reported
  • Liver-relatedAEs in patients with chondrosarcoma were mostly low grade; grade ≥3 liver-related events were reported in 2 patients
  • 1 patient with IDH2-mutant chondrosarcoma died due to hepatic failure
    • It was later discovered that the patient had been self-medicating with high doses of a veterinary antihelminthic that has been linked to hepatic dysfunction
    • This death was temporally associated with INBRX-109 treatment

Efficacy

  • Among evaluable patients (n=31), the disease control rate (DCR) was 87.1% (27/31) (Figure 3)
    • DCR was defined as best overall response of complete response, partial response (PR), or stable disease (SD)
    • Disease control was observed in patients with and without IDH1/IDH2 mutations
  • 2 patients achieved PR (objective response rate, 6.5%), and 25 patients SD (80.6%)
    • Of those who experienced SD, 13 (52.0%) had decreases from baseline in tumor size
  • Clinical benefit was durable: 11 of 27 patients who achieved disease control had a clinical benefit lasting ≥180 days
    • The longest duration of SD was 17.8 months
  • 5 patients were treated for >12 months, including 2 with an IDH1/IDH2 mutation

Figure 3. Best Tumor Response and Time on Treatment

Best responsea

SD

SD

SD

SDb

SDb

PR

SD

SD

SD

SD

SDb

PR

SD

SD

SD

Chondrosarcoma, anyc

SD

IDHmt conventional chondrosarcoma

SDb

SD

Durable disease controld

SDb

Response start

SD

Progressive disease

SD

Patient died

SDb

Patient censored

SD

SDb

Treatment ongoing

NA

PDb

DCR, n (%)

27 (87.1)

PD

PR, n (%)

2 (6.5)

PD

SD

SD, n (%)

25 (80.6)

SDb

SD

0

6

12

18

24

Months

CR, complete response; DCR, disease control rate; IDHmt, isocitrate dehydrogenase 1/2 mutant; NA, not applicable; PD, progressive disease; PR, partial response; SD, stable disease. a A total of 31 patients were included in the analysis. Four patients from cohort B6 were excluded for taking prohibited medications (n=1), not having conventional chondrosarcoma (n=1), or not having first scan data (n=2); b Patient had a mutation in IDH1 (R132) or IDH2 (R172); c One patient was from dose- escalation cohort A4 and received INBRX-109 at a dose of 10 mg/kg; d Durable disease control is SD, PR, or CR for >6 months.

Figure 4. PFS by Kaplan-Meier Analysis

1.0

Chondrosarcoma, anya

0.8

IDHmt conventional

probability

chondrosarcomab

0.4

Median PFS in all groups,

PFS

0.6

7.6 mo (range, 0.03-17.8 mo)

0.2

0.0

0

5

10

15

20

No. at risk

Months

10

4

1

0

23

10

3

2

0

IDHmt, isocitrate dehydrogenase 1/2 mutant; PFS, progression-free survival.

  1. Includes 1 patient from dose-escalation cohort A4 (INBRX-109 10 mg/kg) and 22 patients from dose-expansion cohort B4 (INBRX-109 3 mg/kg); b Two patients were excluded due to taking prohibited medication (n=1) or having dedifferentiated chondrosarcoma (n=1).
  • Median PFS among patients with chondrosarcoma was 7.6 months (range, 0.03-17.8 months; median follow-up, 11.6 months) (Figure 4)
  • The 3- and 6-month PFS rates were 82% and 58%, respectively
  • Median PFS was not reached in the cohort of patients with IDH1/IDH2- mutant conventional chondrosarcoma

Figure 5. Mean Growth Modulation Indexa

2.44

SD

9.87

SD

1.27

SD

4.68

SDb

5.56

SD

1.77

SD

1.13

SD

0.87

SDb

3.93

SD

0.84

SD

0.37

Chondrosarcoma, anyc

SD

0.76

IDHmt conventional

SDb

chondrosarcoma

0.63

SD

Durable disease controld

0.54

SDb

Response start

1.17

SD

Progressive disease

1.47

SDb

Patient died

2.57

NA

Patient censored

0.82

Treatment ongoing

PDb

0.70

PD

1.00

PD

n=23e

SD

0.23

Median GMI, 1.07

SDb

0.26

-12

-6

0

6

12

18

24

Prior treatment

PFS with INBRX-109

duration, mo

treatment, mo

CR, complete response; IDHmt, isocitrate dehydrogenase 1/2 mutant; GMI, growth modulation index; NA, not applicable; PD, progressive disease; PFS, progression-free survival; PR, partial response; SD, stable disease. a Mean GMI as determined by the ratio of PFS with INBRX-109 to prior treatment duration.

Best response on treatment with INBRX-109 is indicated within each bar, and the ratio of PFS with INBRX-109 to prior treatment duration is indicated to the right of each bar; b Patient had a mutation in IDH1 (R132) or IDH2 (R172); c One patient was from dose-escalation cohort A4 and received INBRX-109 at a dose of 10 mg/kg;

  1. Durable disease control is SD, PR, or CR for >6 months. e Overall, 23 of 35 patients were included in this analysis. One patient had a long prior treatment duration of 84 months (cohort B6) and is not included in the figure (GMI, 0.03). Patients were excluded for taking prohibited medications (n=1; cohort B6), not having conventional

chondrosarcoma (n=1; cohort B6), or having a treatment duration that could not be estimated (n=10). Partial start and stop dates were ignored.

  • We also determined the mean growth modulation index (GMI or Von Hoff ratio10) as an exploratory analysis
    • GMI measures tumor growth delay and is considered a way of determining success in studies of sarcoma11
  • Among 23 evaluable patients, the median GMI was 1.07 (range, 0.03-9.87) (Figure 5)
  • Overall, 54.5% of patients experienced a GMI >1, 36.3% a GMI >1.33 (ie, 33% improvement), and 31.8% a GMI >1.5% (ie, 50% improvement)
  • INBRX-109is a third-generation, tetravalent, DR5 agonist precisely engineered for optimal agonism and safety
  • In this phase 1 study of chondrosarcoma, INBRX-109 monotherapy demonstrated potent antitumor activity and led to:
    • High DCR of 87.1%, including 2 PRs
    • Durable clinical benefit in 40.7% of patients
    • Tumor growth delay and decreases in tumor size in a traditionally chemotherapy-resistant disease
    • Median PFS of 7.6 months (historical PFS, <4 months1-3)
  • INBRX-109was well tolerated, with a manageable safety profile
    • Most treatment-related AEs, including liver-related events, were low grade
    • Findings indicate that the INBRX-109 design minimizes hepatotoxicity, unlike earlier DR5 agonists
  • Overall, study results support further evaluation of INBRX-109 as a single agent in unresectable/metastatic chondrosarcoma
    • ChonDRAgon (NCT04950075), a randomized, placebo-controlled, phase 2 trial in conventional chondrosarcoma, is now enrolling (see CTOS 2022 presentation P322 for more information)
    • INBRX-109will also be evaluated in nonconventional chondrosarcoma in cohort B7 of this ongoing phase 1 study

REFERENCES

1.

Livingston JA, et al. Oncotarget. 2016;7(39):64421-64430.

7.

Valley CC, et al. J Biol Chem. 2012;287(25):21265-21278.

2.

Duffaud F, et al. Eur J Cancer. 2021;150:108-118.

8.

Pan L, et al. Cell. 2019;176(6):1477-1489.e14.

3.

van Maldegem A, et al. Oncologist. 2019;24(1):110-116.

9.

Nair PM, et al. Proc Natl Acad Sci U S A.

4.

Miwa S, et al. Int J Mol Sci. 2022;23(3):1096.

2015;112(18):5679-5684.

5.

Walczak H, et al. Nat Med. 1999;5(2):157-163.

10.

Von Hoff DD. Clin Cancer Res. 1998;4(5):1079-1086.

6.

Ashkenazi A, et al. J Clin Invest. 1999;104(2):155-162.

11.

Penel N, et al. Ann Oncol. 2013;24(2):537-542.

ACKNOWLEDGMENTS

  • We thank our patients and participating clinical sites and teams
  • This study is sponsored by Inhibrx, Inc
  • Medical editorial assistance with this presentation was provided by Karen Chinchilla, PhD, of ArticulateScience, LLC, and funded by Inhibrx, Inc

DISCLOSURES

S. P. Chawla received grant support, consulting fees, and/or honoraria from Amgen, Roche, GSK, Threshold Pharmaceuticals, CytRx Corporation, Ignyta, Immune Design, TRACON, Karyopharm Therapeutics, Sarcoma Alliance for Research through Collaboration (SARC), Janssen, Advenchen Laboratories, Bayer, Inhibrx, NKMAX, and TYME and holds stocks or stock options in Aadi Bioscience, Cellestia Biotech, CounterPoint, and Immix Biopharma. A. P. Conley received grant support from the Chordoma Foundation, Chordoma Foundation/CRI, Lilly, National Cancer Institute (NCI), EpicentRx, Inhibrx, and Roche paid to his institution; received consulting fees from Deciphera and Inhibrx; and participated in a data safety monitoring board (DSMB) or advisory board for Applied Clinical Intelligence, Inhibrx, and Aadi Bioscience. C. Lieu received research funding from Merck. B. A. Wilky received consulting fees from Adaptimmune, Adcendo, Daiichi Sankyo, Deciphera, Epizyme, Polaris, SpringWorks, and Boehringer Ingelheim. A. Tolcher received consulting fees (paid to New Experimental Therapeutics, LLC d/b/a NEXT Oncology, of which he is founder and president) from AbbVie, Aclaris Therapeutics, Agenus, Asana BioSciences, Ascentage Pharma, Axlmmune, Bayer, BluPrint Oncology, Daiichi Sankyo, Gilde Healthcare, HBM Partners, IDEA Pharma, Immuneering Corporation, ImmunoMet Therapeutics, IMPACT Therapeutics US, Karma Oncology BV, Kirilys Therapeutics, Lengo Therapeutics, Link Immunotherapeutics, MEKanistic Therapeutics, Menarini Ricerche SpA, Mersana Therapeutics, Nanobiotix, Nerviano Medical Sciences SrI, Nurix Therapeutics, Ocellaris Pharma, Lilly, Partner Therapeutics, Pfizer, Qualigen Therapeutics, Pierre Fabre, Roche, Ryvu Therapeutics, Seagen, SK Life Science, SOTIO Biotech, Spirea Ltd, Sunshine Guojian Pharmaceuticals (Shanghai), Transcenta, Transgene, Trillium Therapeutics, Verastem Oncology, VRise Therapeutics, and Zentalis Pharmaceuticals; received payment for expert testimony from Immunogen; received meeting and travel support (paid to NEXT Oncology) from SOTIO Biotech; participated in an advisory board for Adagene, Aro Biotherapeutics, BioInvent, Boehringer Ingelheim, Deka BioSciences, Eleven Bio, Elucida Oncology, EMD Serono/Merck KGaA, HiberCell, Ikena, Immunome, Janssen Global Services, NBE Therapeutics, Pelican Therapeutics, Jazz Pharmaceuticals, Pieris Pharmaceuticals, Pyxis Oncology, Senti Biosciences, Vincerx Pharma, ZielBio, Zymeworks, Mirati Therapeutics, and Roche; holds patents and/or is on patent applications for Ascentage Pharma and Zentalis Pharmaceuticals; and owns stock or stock options in Pyxis Oncology. J. Chao received research funding from Inhibrx; research funding from Merck and Brooklyn Immunotherapeutics paid to his institution; consulting fees from Lilly, Merck, AstraZeneca, Foundation Medicine, Daiichi Sankyo, MacroGenics, Amgen, Ono Pharmaceutical, Bristol Myers Squibb, Astellas, Turning Point Therapeutics, Silverback Therapeutics, Novartis, Coherus BioSciences, Geneos, Roche, and Guardant Health; speakers bureau honoraria from Merck and Bristol Myers Squibb; and DSMB member fees from Yiviva. N. J. Lakhani received research funding and/or clinical trial costs from Inhibrx, ALX Therapeutics, Ascentage Pharma, Asana BioSciences, BeiGene, Constellation Pharma, Alexion, Cerulean, Forty Seven, Alpine Biosciences, Merck, Pfizer, Regeneron, TaiRx, Apexian, Formation Biologics (Forbius), Symphogen, CytomX, Sapience Therapeutics, Incyte, Jounce, Livzon, Northern Biologics, Innovent Biologics, Ikena, Odonate, Loxo Oncology, Alpine Biosciences, Mersana Therapeutics, MacroGenics, Helsinn, Seagen, Shattuck Labs, Samumed, and Astellas; and participated in an advisory board for and received honoraria from Innovent Biologics and Ikena. M. Diab serves as a consultant for Novartis and Guardant Health. D. Berz received consulting fees from Jazz Pharmaceuticals, Sun Pharma, Biocept, Dare Bioscience, and Oncocyte; payment or honoraria for lectures, presentations, or speakers bureaus, as well as travel support, from AstraZeneca, Caris, Jazz Pharmaceuticals, Oncocyte, and Sun Pharma; and participated in an advisory board for Biocept and Oncocyte. L. Senne, B. O'Neill, M. Fox, and V. Andrianov are employees of and own stock in Inhibrx. B. Eckelman is an employee and shareholder of Inhibrx and holds patents and/or is on patent applications for INBRX-109, a compound from Inhibrx. R. G. Maki is an employee of Peel Therapeutics and received consulting fees and/or honoraria from Bayer, Deciphera, Karyopharm Therapeutics, Peel Therapeutics, TRACON, American Board of Internal Medicine, American Society of Clinical Oncology (ASCO), and UpToDate; received travel support from Bayer and TRACON and received clinical trial support from Amgen, Astex, Boehringer Ingelheim, BioAtla, C4 Therapeutics, Exelixis, Inhibrx, Janssen/PharmaMar, Peel Therapeutics, Rain Therapeutics, Regeneron, Presage, SARC, SpringWorks, and TRACON paid

to his institution. V. Subbiah reports research funding from Inhibrx to conduct clinical trials; other grant support for clinical trials from AbbVie, Agensys, Alfasigma, Altum, Amgen, Bayer, BERG Health, Blueprint Medicines, Boston Biomedical, Boston Pharmaceuticals, Celgene Corporation, D3 Bio, Dragonfly Therapeutics, Exelixis, Fujifilm, GSK, Idera Pharmaceuticals, Incyte, Inhibrx, Loxo Oncology/ Lilly, MedImmune, MultiVir, NanoCarrier, National Comprehensive Cancer Network, NCI-CTEP, Novartis, PharmaMar, Pfizer, Relay Therapeutics, Roche/Genentech, Takeda, Turning Point Therapeutics, The University of Texas MD Anderson Cancer Center, and Vegenics; travel support from ASCO, European Society for Medical Oncology, Helsinn, Incyte, Novartis, and PharmaMar; consultancy or advisory board participation for Helsinn, Incyte, Loxo Oncology/Lilly, MedImmune, Novartis, QED Therapeutics, Relay Therapeutics, Daiichi Sankyo, and R-Pharm US; and other

relationship with Medscape.

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Presented at the Connective Tissue Oncology Society 2022 Annual Meeting; November 16-19, 2022; Vancouver, BC, Canada

Sponsored by Inhibrx, Inc

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