A first-in-class RNA degrader reduces c-MYC expression and myeloma cell survival in preclinical models

D Domenico Maisano (Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States) T Tenghui Wang (Skaggs Graduate School of Chemical and Biological Sciences) S Steffen Benham Kulp (Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School. 02215 Boston, MA, United States) V Vanessa Katia Favasuli (Candiolo Cancer Institute, FPO-IRCCS, Candiolo (TO), Italy) Y Yuquan Tong (The Scripps Research Institute, Department of Chemistry, 130 Scripps Way, Jupiter, Florida 33458, United States) M Michela Cumerlato (Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, United States) C Chungen Li F Francesca Barello (Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, United States) M Marcello Turi (Candiolo Cancer Institute FPO-IRCCS, Candiolo, Italy) P Paola Rampa (INOC - Istituto Nazionale Oncologico Candiolo, Candiolo (TO), Italy) R Rosa Alba Parisi (Candiolo Cancer Institute, FPO-IRCCS, Candiolo (TO), Italy) F Filip Garbicz F Francesco Ladisa (Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States) G Giulia Giorgetti (Clinic of Hematology, Department of Internal Medicine and Medical Specialties (DiMI), University of Genoa, Genoa, Italy) C Chandraditya Chakraborty (Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States) L Laure Vreux (Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States) V Valentina Sangiorgio (Candiolo Cancer Institute, FPO-IRCCS, Candiolo (TO), Italy) I Ivana Sarotto (Candiolo Cancer Institute FPO-IRCCS, Candiolo, Italy) A Anil Aktas Samur (Dana Farber Cancer Institution, Boston, Massachusetts, United States) M Mehmet K. Samur (Dana-Farber Cancer Institute and Harvard School of Public Health, Boston, Massachusetts, United States) R Ruben D. Carrasco (Department of Pathology, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, United States) M Mariateresa Fulciniti (Dana Farber Cancer Institute, Boston, Massachusetts, United States) M Michael D Cameron (The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, Florida, United States) K Kenneth C. Anderson A Annamaria Gulla (Istituto nazionale Oncologico Candiolo INOC, Candiolo, Italy) J Jessica Childs-Disney (The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Department of Chemistry, Jupiter, Florida, United States) M Matthew D. Disney (Department of Chemistry, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, 130 Scripps Way, Jupiter, Florida 33458, United States) E Eugenio Morelli (INOC - Istituto Nazionale Oncologico Candiolo, Candiolo, Italy) N Nikhil C. Munshi

Abstract

The c-MYC (MYC) oncogene is a critical driver of multiple myeloma (MM), however, direct targeting of the MYC protein has proven challenging due to its intrinsic structural disorder. In this study, we evaluated the biological activity and molecular mechanism of a ribonuclease-targeting chimera (RiboTAC) designed to promote the degradation of MYC mRNA (MYC-RiboTAC) across a panel of primary patient MM samples and MM cell lines. This heterobifunctional molecule consists of a small molecule targeting the MYC internal ribosomal entry site (IRES) conjugated to a small-molecule recruiter of endogenous RNaseL. The MYC-RiboTAC reduces MYC mRNA and protein levels in an RNase L-dependent manner, selectively inhibits MYC-driven transcriptional programs, and exhibits potent anti-MM activity. It effectively suppresses cell growth in MM cells co-expressing MYC and RNase L, even in the presence of the protective bone marrow. Furthermore, it synergizes with clinically active agents such as carfilzomib, lenalidomide, and pomalidomide. Importantly, MYC-RiboTAC displays favorable safety and pharmacokinetic profiles in mice and significantly suppresses tumor growth in NOD SCID mice bearing MM xenografts, as shown in two different models. These findings highlight the potential of RNA degraders to target mRNAs encoding "undruggable" proteins such as MYC, offering a promising avenue for precision cancer therapy

Article Details

Journal Blood
Volume / Issue Vol. 1, Issue 1
Published July 29, 2026
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (29)

D

Domenico Maisano

Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States

T

Tenghui Wang

Skaggs Graduate School of Chemical and Biological Sciences

S

Steffen Benham Kulp

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School. 02215 Boston, MA, United States

V

Vanessa Katia Favasuli

Candiolo Cancer Institute, FPO-IRCCS, Candiolo (TO), Italy

Y

Yuquan Tong

The Scripps Research Institute, Department of Chemistry, 130 Scripps Way, Jupiter, Florida 33458, United States

M

Michela Cumerlato

Department of Medical Oncology, Dana-Farber Cancer Institute, 450 Brookline Avenue, Boston, MA 02215, United States

C

Chungen Li

F

Francesca Barello

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, United States

M

Marcello Turi

Candiolo Cancer Institute FPO-IRCCS, Candiolo, Italy

P

Paola Rampa

INOC - Istituto Nazionale Oncologico Candiolo, Candiolo (TO), Italy

R

Rosa Alba Parisi

Candiolo Cancer Institute, FPO-IRCCS, Candiolo (TO), Italy

F

Filip Garbicz

F

Francesco Ladisa

Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States

G

Giulia Giorgetti

Clinic of Hematology, Department of Internal Medicine and Medical Specialties (DiMI), University of Genoa, Genoa, Italy

C

Chandraditya Chakraborty

Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States

L

Laure Vreux

Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts, United States

V

Valentina Sangiorgio

Candiolo Cancer Institute, FPO-IRCCS, Candiolo (TO), Italy

I

Ivana Sarotto

Candiolo Cancer Institute FPO-IRCCS, Candiolo, Italy

A

Anil Aktas Samur

Dana Farber Cancer Institution, Boston, Massachusetts, United States

M

Mehmet K. Samur

Dana-Farber Cancer Institute and Harvard School of Public Health, Boston, Massachusetts, United States

R

Ruben D. Carrasco

Department of Pathology, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115, United States

M

Mariateresa Fulciniti

Dana Farber Cancer Institute, Boston, Massachusetts, United States

M

Michael D Cameron

The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Jupiter, Florida, United States

K

Kenneth C. Anderson

A

Annamaria Gulla

Istituto nazionale Oncologico Candiolo INOC, Candiolo, Italy

J

Jessica Childs-Disney

The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, Department of Chemistry, Jupiter, Florida, United States

M

Matthew D. Disney

Department of Chemistry, The Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, 130 Scripps Way, Jupiter, Florida 33458, United States

E

Eugenio Morelli

INOC - Istituto Nazionale Oncologico Candiolo, Candiolo, Italy

N

Nikhil C. Munshi