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Type
Original Research
PAGE NO.
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10.37547/tajiir/Volume07Issue07-02
OPEN ACCESS
SUBMITED
25 June 2025
ACCEPTED
30 June 2025
PUBLISHED
05 July 2025
VOLUME
Vol.07 Issue 07 2025
CITATION
Oleksandra Bondarenko. (2025). Targeted Degradation of MYB as a Novel
Therapeutic Strategy for Acute Myeloid Leukemias. The American Journal
of Interdisciplinary Innovations and Research, 7(07), 8
–
15.
https://doi.org/10.37547/tajiir/Volume07Issue07-02
COPYRIGHT
© 2025 Original content from this work may be used under the terms
of the creative commons attributes 4.0 License.
Targeted Degradation of
MYB as a Novel
Therapeutic Strategy for
Acute Myeloid Leukemias
Oleksandra Bondarenko
Boston, Massachusetts, USA
Abstract:
This study examines targeted degradation of
the transcription factor MYB as a novel therapeutic
avenue in acute myeloid leukemias. Its relevance stems
from the limited efficacy of existing treatment regimens
and the emergence of drug‐resistant disease form
s. The
work’s novelty lies in the integrated comparison of
genetic models for MYB destabilization, chemical dTAG
approaches, and the repurposing of low-molecular-
weight compounds mebendazole and vitaferin A. Data
are synthesized on MYB’s transformational p
roperties
critical
for
leukemic-clone
maintenance,
and
experimental findings are reviewed on the suppression
of transcriptional programs and induction of blast-cell
death following complete factor elimination. Special
attention is devoted to prospects for developing
PROTAC degraders and molecular glues capable of
catalyzing ubiquitin-dependent proteolysis of MYB at
low compound doses. The research aims to construct a
comprehensive assessment of the efficacy and safety of
MYB-degradation strategies and to identify directions
for further preclinical investigation. Methods include
comparative analysis of peer-reviewed literature, critical
appraisal of in vitro and in vivo data, and synthesis of
pharmacodynamic profiles of the repurposed agents.
The overall eval
uation highlights the approach’s
potential to overcome therapeutic resistance and
improve patient survival. The findings will interest
pharmacologists, oncologists, clinical researchers, and
specialists in chemical biology.
Keywords:
acute myeloid leukemia, MYB, proteasomal
degradation, PROTAC, mebendazole, vitaferin A,
targeted therapy, ubiquitin, molecular glue, drug
resistance
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INTRODUCTION
Acute myeloid leukemia (AML) remains a challenging
disease to cure: escalating chemotherapy regimens no
longer improve outcomes, prompting researchers to
focus on selectively suppressing factors that sustain
blast proliferation. The transcription factor MYB, which
governs
self-renewal
and
differentiation
of
hematopoietic stem cells, becomes hyperactivated in
certain contexts
—particularly in MLL‐rearranged
leukemias
—
forming pathogenic expression networks
that block maturation and drive unchecked growth. In
experimental models, MYB elimination induces
leukemic‐cell death, designating this protein as a high‐
priority target for novel therapeutic development.
Early intervention strategies aimed to disrupt the MYB
–
CBP/P300 complex: natural triterpenoids celastrol and
plumbagin, alongside synthetic naphthol derivatives,
impeded coactivator recruitment, weakened the
transcriptional
program,
and
inhibited
blast
proliferation. A more radical approach employed the
cell‐penetrating peptidomimetic MYBMIM, designed on
the basis of the crystal structure of the interaction
interface; MYBMIM displaces MYB from its complex,
downregulates MYC and BCL2 expression, and triggers
apoptosis. In mice bearing human AML xenografts, this
compound slowed disease progression and extended
survival. Despite these encouraging outcomes, MYB
remains present in the nucleus under this strategy,
limiting the depth of the antitumor effect.
The concept of induced proteolysis ultimately enables
complete MYB removal: heterobifunctional PROTAC
molecules simultaneously bind the target and an E3
ubiquitin ligase, initiate polyubiquitination, and shuttle
the protein to the proteasome, acting repeatedly in a
catalytic fashion. Such kinetics promise profound and
durable remissions at low doses by eradicating the
source of the transformational signal and bypassing
resistance mechanisms that arise from partial inhibition.
Consequently, targeted degradation of MYB is regarded
as the most promising avenue for creating
fundamentally new AML therapies.
The urgency of this topic is driven by the critical need for
treatments against chemoresistant AML variants and
the emergence of initial encouraging data on MYB
suppression in disease models. The aim of this article is
to analyze the current literature on targeted MYB
degradation as an AML treatment strategy, to evaluate
the scientific findings to date, and to outline prospects
for its application. The specific objectives are:
1.
To synthesize data on MYB’s role in AML
pathogenesis and on prior therapeutic attempts
targeting MYB;
2.
To
describe
key
experimental
discoveries demonstrating the feasibility of induced
MYB degradation and its effects on leukemia;
3.
To discuss the therapeutic potential of
proteasomal‐degradation technologies in comparison
with conventional treatment modalities;
4.
To assess the outlook for integrating
MYB‐degradation approaches into preclinical research
and clinical practice.
METHODS AND MATERIALS
Z. Anwar [1] delivered a systematic review of degrader
prospects in leukemia, underscoring the catalytic
mechanism inherent to the PROTAC approach. M.
Bekesh [2] examined the evolution of the PROTAC
platform and its target-selection criteria, identifying
transcription factors as the most promising candidates.
K. Klesham [3] experimentally validated the efficacy of
vitaferin A in eliminating MYB within AML cell models. T.
Harada [4] developed a dTAG system for rapid
degradation of endogenous MYB and assessed the
transcriptomic consequences of factor removal. F.
Modman [5] described mebendazole’s anti
-MYB effects,
demonstrating its potential in preclinical studies. K.
Ramaswami [6] engineered the peptidomimetic
MYBMIM and proved that displacing MYB from its p300
complex triggers blast-cell apoptosis. R. G. Ramsey [7]
investigated MYB’s roles in normal hematopoiesis
and
oncogenesis, thereby substantiating its therapeutic
appeal. V. Walf-Vorderwülbecke [8] showed that drug-
induced degradation of MYB suppresses leukemia
progression in vivo.
In preparing this article, comparative and analytical
methods were employed, coupled with a critical
synthesis of data from peer-reviewed publications,
bibliographic searches in PubMed and Web of Science,
and conceptual modeling of PROTAC technologies’
potential for clinical translation.
RESULTS
Accumulating evidence confirms that AML cells are
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critically dependent on sustained MYB expression.
Genetic deletion or silencing of MYB induces rapid
leukemic-cell death, as demonstrated in both classical
knockout models and modern induced-degradation
systems. In a recent study, researchers employed the
chemical-degron technology (dTAG system) to
selectively eradicate endogenous MYB in AML cells. By
fusing the FKBP12^F36V degron domain to the C-
terminus of MYB in the MV4-11 cell line, subsequent
treatment with the selective ligand dTAGV-1 triggered
rapid, ubiquitin-dependent proteolysis of the tagged
MYB protein. Within one hour of degrader addition,
cellular MYB levels had plummeted to near zero.
Predictably, such acute depletion of MYB resulted in a
dramatic loss of viability among leukemic cells, mirroring
the effects seen in genetic MYB knockouts [4].
Simultaneously, transcriptome analysis via SLAM-seq
revealed that removal of MYB altered transcription rates
of hundreds of genes, with predominant suppression of
those directly regulated by MYB. Notably, transcripts of
MYC, BCL2, and other MYB-dependent proto-oncogenes
were significantly reduced following MYB degradation
[6].
Thus, the in vitro induced-degradation experiment
vividly demonstrated that the oncogenic program in
AML cells collapses upon MYB elimination, leading to
clonal demise. These results substantiate the rationale
for identifying compounds capable of effecting selective
MYB degradation as a therapeutic avenue (Figure 1).
Figure 1. Major categories of proteins for which the PROTAC strategy demonstrates the greatest therapeutic
efficacy [2]
Figure 1 illustrates six classes of targets that are optimal
for proteasomal degradation. MYB falls into two of these
groups
—“undruggable” transcription factors and
scaffold
(platform)
proteins.
Such
positioning
strengthens the case for choosing MYB as a therapeutic
target and sets the stage for the development of
selective degraders described below.
Induction of MYB proteasomal degradation by drug
Tenets of
PROTAC
targets
Resistance
mutations
Undruggable
Scaffolding
function
Gene
amplification/
protein
overexpressi
on
Isoform
expression or
localization
Protein
aggregates
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repurposing. The first chemical breakthrough in
targeting MYB arose from a drug-repurposing strategy.
By comparing the gene-
expression “signature” governed
by MYB against transcriptomic profiles in the
Connectivity Map, researchers identified compounds
capable of dampening the MYB signature. One of the
strongest “hits” was mebendazole, a long
-standing
benzimidazole
antihelminthic.
In
AML
cells,
mebendazole unexpectedly reduced c-Myb protein
levels, effectively inducing its degradation via the
proteasome. Mechanistically, mebendazole disrupts the
HSP70/HSC70 chaperone system required for MYB
stability, triggering ubiquitination and proteasomal
clearance of c-Myb [8].
Notably, this effect occurs with only transient exposure:
even brief mebendazole treatment markedly impaired
leukemic-blast colony formation, while normal
hematopoietic progenitors from cord blood remained
largely unaffected. This suggests a therapeutic window
in which leukemic cells are more susceptible to MYB loss
than their normal counterparts. In vivo experiments in a
human AML xenograft model further validated
mebendazole’s promise: treated mice exhibited
significantly slower disease progression compared with
untreated controls [8]. Moreover, given mebendazole’s
extensive, well-tolerated use in humans for parasitic
infections, these data support induced MYB degradation
by mebendazole as a novel and potentially safe AML
therapy [8].
Another repurposed agent that elicits targeted MYB loss
is withaferin A (WFA), a steroidal lactone derived from
the plant Withania known for its antitumor properties.
WFA emerged as a top hit alongside mebendazole in the
Connectivity Map screen for MYB-suppressive activity.
Recent work has shown that WFA induces rapid and
pronounced ablation of c-Myb in AML cells [3]. Within
hours of treatment, MYB protein levels fall to nearly
undetectable levels and transcription of MYB-target
genes is suppressed. WFA treatment mirrors
mebendazole’s effects, triggering blast
-cell death and
inhibiting colony formation. Its mechanism likewise
involves proteostasis stress: WFA activates the
unfolded-protein
response,
destabilizing
the
HSP70/HSC70 complex and leading to c-Myb
ubiquitination and degradation. Crucially, expression of
a degradation-resistant MYB mutant partially rescues
cells from WFA-induced death, confirming the specificity
of this pathway [3].
Thus, WFA’s antileukemic action is largely mediated
through MYB depletion. In vivo, WFA treatment of AML-
bearing mice slowed disease progression and reduced
leukemic burden. Given WFA’s historical use in
traditional medicine and established human exposure,
its repurposing for AML therapy represents a highly
attractive direction [3].
A distinguishing feature of the MYB-degradation
strategy is the complete removal of the oncoprotein
from the cell, whereas traditional approaches merely
block its function while leaving the protein intact.
Experience with direct MYB inhibitors shows their
limited efficacy due to incomplete target suppression
and off-target effects. For instance, small molecules that
disrupt the MYB
–
p300 interaction (celastrol, plumbagin,
etc.) and the peptidomimetic MYBMIM partially inhibit
MYB’s transcriptional activity and slow leukemic
-cell
growth [6]. However, a recent comparative analysis of
these agents revealed significant drawbacks: purported
MYB inhibitors exhibit only partial specificity and induce
substantial collateral effects on the expression of
unrelated genes. Moreover, some of these compounds
were unexpectedly found to act in a dual manner
—
alongside inhibiting certain MYB functions, they
paradoxically stimulate the expression of other MYB-
regulated genes, functioning as mixed agonist
–
antagonists. These unforeseen activities complicate the
clinical use of direct MYB inhibitors [6].
In contrast, targeted degradation eliminates MYB as a
factor, theoretically obviating the risk of residual protein
exerting excessive or compensatory activity. Indeed, in
the described models, treatment with degraders
(mebendazole, WFA) yielded unequivocal suppression
of MYB-driven transcriptional programs and rapid cell
death, with no signs of paradoxical oncogenic pathway
activation [3; 8]. These findings suggest that a
degradation-based strategy may be both more effective
and more specific than traditional MYB inhibitors.
Different pharmacological paradigms vary in their
specificity and clinical applicability. Comparing the
approaches reported in the literature allows an
assessment of the potential gains from adopting
targeted-degradation technologies (Table 1).
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Table 1
–
Comparative analysis of therapeutic approaches in AML (compiled by the author based on [1
–
8])
Approach
Target
Mode of
Action
Selectivity
Advantages
Limitations
Chemotherapy
DNA
synthesis
Cytotoxicity
Low
Effective against
rapidly dividing
cells
Myelosuppression;
resistance
FLT3 inhibitors
Activated
kinase
Enzymatic
blockade
Medium
Subtype-specific
activity
Secondary
mutations
MYB
–
p300
interaction
inhibitors
Protein
–
protein
Coactivator
disruption
Medium
Disrupts
transcriptional
complex
Partial
MYB
suppression;
off-
target effects [6]
Mebendazole/WFA
repurposing
MYB
Induced
degradation
High
Uses
approved
drugs;
known
safety profiles
Dose-dependent
off-target activity
[3; 8]
PROTAC degraders
targeting MYB
MYB
Proteasomal
degradation
Very high
Catalytic action
at low doses
Requires
pharmacokinetic
optimization
Comparison shows that MYB removal outperforms
traditional regimens both in selectivity and depth of
tumor-clone suppression. This advantage stems from
the leukemic cell’s inability to compensate for loss of
a
central transcriptional node, whereas kinase inhibition
often leads to escape signaling.
In summary, the review of experimental data
demonstrates the practical feasibility and high efficacy
of targeted MYB degradation in AML models. Induced
proteasomal elimination of MYB
—
whether via
dedicated chemical degraders or repurposed agents
—
triggers collapse of the oncogenic program and
eradication of leukemic cells in vitro and in vivo. These
findings lay the groundwork for developing a new class
of therapeutics aimed at eliminating MYB in resistant
AML forms.
DISCUSSION
The findings presented here must be viewed in the
context of developing novel antileukemic therapies.
Targeted
degradation
of
MYB
represents
a
fundamentally different strategy, aimed at the root of
the oncogenic process
—
the pathological transcriptional
network sustained by MYB. Unlike traditional cytotoxic
agents, which nonspecifically target dividing cells, or
kinase inhibitors that block individual signaling
pathways, eradication of a key transcription factor
promises simultaneous suppression of multiple
oncogenic gene targets. In the case of MYB, these
include critical drivers of proliferation and survival (such
as MYC and BCL2) as well as factors that inhibit cellular
differentiation. Consequently, MYB removal can induce
both differentiation and apoptosis of leukemic blasts, as
experimentally evidenced by mitochondrial apoptotic
markers and signs of cellular maturation upon MYB
suppression. This multi-targeted impact on the gene
network renders MYB degradation a potent weapon
against leukemia, potentially surpassing traditional
modalities in depth of effect.
Thus, MYB degradation effectively “knocks out” the
central hub upon which the malignant clone depends, a
scenario fundamentally distinct from the action of
narrowly focused agents (e.g., FLT3 or IDH mutation
inhibitors), whose efficacy is confined to tumor
subpopulations and often wanes with the emergence of
secondary mutations. By contrast, MYB elimination
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theoretically leaves leukemic cells no compensatory
route, as it concurrently disrupts multiple oncogenic
pathways.
From a practical standpoint, the targeted-degradation
platform is advancing rapidly and already moving
beyond the confines of the laboratory. PROTAC
technology, as noted, has given rise to numerous
experimental degraders against various oncoproteins
[1]. Notably, the first examples are now appearing in
oncohematology: PROTACs targeting the proto-
oncogene STAT3, oncogenic kinases, and epigenetic
regulators are under development, with several
progressing through preclinical evaluation. Although no
MYB-specific PROTAC has yet been disclosed, all the
elements for its design are in place. As a “warhead”—
the
binding
moiety
—
one
might
employ
the
peptidomimetic MYBMIM or another small molecule
that disrupts the MYB
–
p300 interaction. By linking such
a ligand to an appropriate linker and an E3-ligase
recruiting moiety (for example, CRBN or VHL), it would
be possible to craft a bifunctional degrader capable of
recruiting the E3 ligase to MYB and marking it for
proteasomal destruction. Given the success of PROTACs
in other models, a parallel approach against MYB is
anticipated to yield a potent antileukemic agent.
The PROTAC system has opened the door to the
selective elimination of nuclear oncoproteins once
considered “undruggable” by conventional small
-
molecule inhibitors. A chimeric PROTAC simultaneously
engages the target factor and an E3 ligase, forming a
transient
ternary
complex
that
initiates
polyubiquitination
and
subsequent
proteasomal
degradation (Figure 2).
Figure 2. Sequence of events in PROTAC-
induced MYB degradation: disease → target → tool → proteasomal
removal → blast differentiation and apoptosis (compiled by the author based on [2])
Comparing the proposed strategy with conventional
AML treatments highlights several aspects. Standard
chemotherapy
—
based
on
antimetabolites
and
cytotoxins
—
lacks molecular specificity: it attacks all
rapidly dividing cells, causing severe side effects and
failing to guarantee eradication of the leukemic clone,
particularly when the tumor harbors stem cells with low
proliferative
activity.
Allogeneic
bone-marrow
transplantation can achieve radical cure through graft-
versus-leukemia immunity but entails high mortality and
serious complications. Targeted agents against mutant
tyrosine kinases (for example, FLT3 inhibitors) and
[Chemoresistant ALL]
↓
[MYB - pathologic transcriptional network node]
↓
[PROTAC-degrador: WARHEAD-linker-E3]
↓
[MYB proteasomal elimination]
↓
[↓ MYC, BCL2 → blast differentiation and apoptosis]
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epigenetic enzymes (IDH1/2 inhibitors) benefit only the
corresponding patient subgroups and, while they often
induce remission, do not prevent relapse when used as
monotherapy. Against this backdrop, the MYB-
degradation
strategy
distinguishes
itself
by
universality
—
MYB is active across many AML subtypes,
including cases without “druggable” mutations.
Moreover, it directly targets the fundamental
mechanism sustaining leukemia. Of course, risks must
be acknowledged: MYB is essential for normal
hematopoiesis, so systemic MYB suppression may lead
to myelosuppression and aplastic states. However,
hematologists are accustomed to this challenge
—
intensive chemotherapy likewise ablates bone marrow,
and clinicians manage the effect via transplantation or
growth-factor support.
From the standpoint of in vivo efficacy and clinical
translation, the first positive signals have already
emerged. Mebendazole repurposing advanced rapidly
to clinical evaluation thanks to its prior approval for
other indications. In particular, clinical trials combining
mebendazole with low-dose cytarabine in elderly and
refractory AML patients are being initiated [5]. This
regimen is designed to harness synergy: mebendazole
both directly undermines blast survival through MYB
(and other factor) degradation and increases residual
cells’ sensitivity to chemotherapeutics.
PROTAC platform technologies are already in early
clinical studies for a variety of targets
—
such as
androgen-receptor degraders in prostate cancer and
estrogen-receptor degraders in breast cancer [2]. In
oncohematology, efforts are also underway: for
example, a PROTAC against BCL-XL, intended to treat
leukemias without platelet toxicity, and degraders of
fusion oncoproteins have been announced. Although
specific data on a MYB-targeting PROTAC have not yet
appeared, successes in related fields make the
development of such molecules highly likely.
Preclinically, they could be evaluated in human AML
xenografts in immunodeficient mice (PDX models),
where MYBMIM, mebendazole, and WFA have already
demonstrated proof of concept.
CONCLUSION
The advancement of a targeted MYB-degradation
strategy heralds a new chapter in acute myeloid
leukemia therapy. Existing studies compellingly
demonstrate the scientific merit of this approach: they
confirm MYB’s central role in maintaining the malignant
AML phenotype and show that MYB elimination halts
proliferation and induces leukemic-cell death. From a
practical standpoint, MYB degradation offers an
innovative solution to overcome drug resistance. In
cases where tumors fail to respond to chemotherapy,
direct removal of the transcriptional oncogene may
deliver a “knockout” blow from which c
ancer cells
cannot recover. This is especially relevant in refractory
AML subtypes, where alternative targets may be absent
or play only secondary roles.
In vitro and in vivo data indicate that proteasomal
clearance of MYB achieves selective eradication of the
leukemic clone while sparing normal hematopoietic
progenitors to a large extent. These findings provide
strong justification for continued development of this
approach. Repurposing existing agents (such as
mebendazole) accelerates the transition to clinical
evaluation, while emerging platforms (PROTACs,
molecular glues) expand the toolkit for directing the
proteasome against MYB. Integration of MYB-
degradation strategies into the preclinical pipeline is
already underway: advanced animal studies are in
progress,
and
combination
regimens
with
chemotherapy are being optimized. In the near term,
initial clinical trial results can be expected to clarify the
feasibility and efficacy of this approach in patients.
In summary, targeted MYB degradation has established
itself as a promising AML treatment modality capable of
complementing and potentially surpassing conventional
regimens in resistant disease forms. If subsequent trials
confirm the safety and effectiveness of MYB
degradation, this strategy may assume a prominent
place in the antileukemic armamentarium
—
paving the
way to more durable remissions and cures for patients
who have exhausted existing options.
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