Art. -Nr.: HY-170451

Seldegamadlin

Name: Seldegamadlin
Brand: MedChemExpress
SKU: HY-170451
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(Synonyms: KT-253)

1 Cited Publications

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Seldegamadlin (KT-253) is a cereblon-recruiting PROTAC degrader of MDM2, with a DC₅₀ of 0.4 nM. Seldegamadlin catalyzes the ubiquitination and proteasomal degradation of MDM2, disrupts the MDM2/p53 autoregulatory feedback loop, induces apoptosis, caspase activation and p53 target gene expression, and inhibits the growth of wild-type p53 hematologic tumor cells and solid tumor cells. Seldegamadlin is applicable for the research of acute myeloid leukemia, acute lymphoblastic leukemia, diffuse large B-cell lymphoma and wild-type p53 solid tumors.
(Pink: MDM-2/p53 ligand (HY-170452); Blue: Cereblon ligand (HY-163927); Black: linker (HY-W001478)).

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Reinheit: 98.53%
CAS. Nr.: 2713618-08-5
Formel: C₄₈H₅₂Cl₂FN₇O₆
Molecular Weight:912.87

Speicherung:

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Seldegamadlin Chemical Structure

CAS. Nr.: 2713618-08-5

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Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (1)
Lösungsmittel & Löslichkeit
- In Vitro
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

Seldegamadlin (KT-253) is a cereblon-recruiting PROTAC degrader of MDM2, with a DC₅₀ of 0.4 nM. Seldegamadlin catalyzes the ubiquitination and proteasomal degradation of MDM2, disrupts the MDM2/p53 autoregulatory feedback loop, induces apoptosis, caspase activation and p53 target gene expression, and inhibits the growth of wild-type p53 hematologic tumor cells and solid tumor cells. Seldegamadlin is applicable for the research of acute myeloid leukemia, acute lymphoblastic leukemia, diffuse large B-cell lymphoma and wild-type p53 solid tumors^[1]^[2]. (Pink: MDM-2/p53 ligand (HY-170452); Blue: Cereblon ligand (HY-163927); Black: linker (HY-W001478)).

IC₅₀ & Target

^[1]

MDM2

0.4 nM (DC₅₀)

Alle PROTACs Isoform-spezifische Produkte anzeigen :

Cellular Effect

Cell Line	Type	Value	Description	References
HEK-293T	DC₅₀	0.4 nM	MDM2 degradation in HEK293T-HiBiT cells stably transfected with C-terminal HiBiT-tagged MDM2, measured via luciferase signal using the Nano-Glo HiBiT lytic detection system after 4 hours of incubation. MDM2 degradation in HEK293T-HiBiT cells stably transfected with C-terminal HiBiT-tagged MDM2, measured via luciferase signal using the Nano-Glo HiBiT lytic detection system after 4 hours of incubation.	39648478
RS4-11	IC₅₀	0.3 nM	Cell growth inhibition against human RS4;11 acute lymphoblastic leukemia cells. Cell growth inhibition against human RS4;11 acute lymphoblastic leukemia cells.	39648478
RS4-11	EC₅₀	0.05 nM	p53 stabilization in human RS4;11 acute lymphoblastic leukemia cells. p53 stabilization in human RS4;11 acute lymphoblastic leukemia cells.	39648478
RS4-11	IC₅₀	< 0.1 nM	Growth inhibition against p53 wild-type RS4;11 (B-cell ALL) cells. Growth inhibition against p53 wild-type RS4;11 (B-cell ALL) cells.	39648478
MV4-11	IC₅₀	0.04 nM	Growth inhibition against p53 wild-type MV4;11 (AML) cells. Growth inhibition against p53 wild-type MV4;11 (AML) cells.	39648478
OCI-LY19	IC₅₀	0.5 nM	Growth inhibition against p53 wild-type OCI-Ly19 (ABC-DLBCL) cells. Growth inhibition against p53 wild-type OCI-Ly19 (ABC-DLBCL) cells.	39648478
EOL1	IC₅₀	0.6 nM	Growth inhibition against p53 wild-type EOL-1 (AML) cells. Growth inhibition against p53 wild-type EOL-1 (AML) cells.	39648478
OCI-AML-5	IC₅₀	1.1 nM	Growth inhibition against p53 wild-type OCI-AML-5 (AML) cells. Growth inhibition against p53 wild-type OCI-AML-5 (AML) cells.	39648478
MOLM-13	IC₅₀	1.6 nM	Growth inhibition against p53 wild-type MOLM-13 (AML) cells. Growth inhibition against p53 wild-type MOLM-13 (AML) cells.	39648478
OCI-AML2	IC₅₀	> 10 nM	Growth inhibition against p53 wild-type OCI-AML-2 (AML) cells. Growth inhibition against p53 wild-type OCI-AML-2 (AML) cells.	39648478
OCI-AML-3	IC₅₀	> 100 nM	Growth inhibition against p53 wild-type OCI-AML-3 (AML) cells. Growth inhibition against p53 wild-type OCI-AML-3 (AML) cells.	39648478

In Vitro

Seldegamadlin (KT-253) (150 nM; 60 min) degrades MDM2 to undetectable levels in MV4;11 acute myeloid leukemia (AML) cells within 60 minutes^[1].
Seldegamadlin (20 nM; 2-8 h) selectively upregulates p53 and its downstream target proteins in RS4;11 acute lymphoblastic leukemia (ALL) cells without off-target degradation effects [1].
Seldegamadlin (1.8 nM; 2-4 h) degrades MDM2 to undetectable levels in RS4;11 ALL cells within 4 hours^[1].
Seldegamadlin (150 nM; 15-60 min) induces an 84% knockdown of MDM2 at 15 minutes and a 91% degradation of MDM2 at 60 minutes in RS4;11 acute lymphoblastic leukemia (ALL) cells^[1].
MDM2 inhibitor (0.01-10000 nM; 2 h) stabilizes p53 in RS4;11 acute lymphoblastic leukemia (ALL) cells, with an EC₅₀ of 0.05 nM after 2 hours of treatment^[1].
Seldegamadlin (0.1-10000 nM; 8 h) induces a dose-dependent upregulation of mRNA levels of p53 target genes in RS4;11 acute lymphoblastic leukemia (ALL) cells^[1].
Seldegamadlin (0.1-10000 nM) exerts no growth inhibitory effect on hematologic tumor cell lines harboring mutant p53 (TMD8, THP-1, Kasumi-1, Kasumi-6, LP-1, MOLP-2)^[1].
Seldegamadlin (0.01-1000 nM; 4 h) degrades MDM2 in HEK293T-HiBiT cells, with a DC₅₀ of 0.4 nM^[1].
Seldegamadlin (0.01-1000 nM) inhibits the proliferation of RS4;11 acute lymphoblastic leukemia (ALL) cells, with an IC₅₀ of 0.3 nM^[1].
Seldegamadlin (1-1000 nM; 48 h) induces caspase-dependent apoptosis in RS4;11 acute lymphoblastic leukemia (ALL) cells within 48 hours^[1].
Seldegamadlin (1-10000 nM; 96 h for growth inhibition; 48 h for apoptosis) induces potent growth inhibition and apoptosis in a variety of p53 wild-type hematologic and solid tumor cell lines^[1].
Seldegamadlin (0.01-10 nM), when combined with 1.6 μM Venetoclax (HY-15531), enhances apoptosis of MOLM-13 acute myeloid leukemia (AML) cells and exerts maximal growth inhibition on MOLM-13 acute myeloid leukemia (AML) cells^[1].
MCL-1 inhibitor (1-1000 nM; 4 h) depletes S-phase cells and induces robust apoptosis in RS4;11 acute lymphoblastic leukemia (ALL) and MV4;11 acute myeloid leukemia (AML) cells^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis^[1]

Cell Line:

RS4;11 acute lymphoblastic leukemia (ALL) cells
Concentration:

1.8 nM
Incubation Time:

2, 4 h
Result:

Reduced MDM2 protein levels to undetectable levels within 4 hours.

Apoptosis Analysis^[1]

Cell Line:

RS4;11 acute lymphoblastic leukemia (ALL) cells
Concentration:

1, 10, 100, 1000 nM
Incubation Time:

4 h
Result:

Induced dose-dependent caspase 3/7 activation over 48 hours, with higher activation seen at higher concentrations.

Real Time qPCR^[1]

Cell Line:

RS4;11 acute lymphoblastic leukemia (ALL) cells
Concentration:

0.1, 1, 10, 100, 1000 nM
Incubation Time:

8 h
Result:

Induced a dose-dependent increase in relative mRNA levels of p53 target genes (MDM2, GDF15, CDKN1A, GADD45A, TNFRSF10B, FAS, BBC3), with an approximate fourfold increase at 10 nM and eightfold or greater increase at 1000 nM.

Cell Cycle Analysis^[1]

Cell Line:

RS4;11 acute lymphoblastic leukemia (ALL) cells, MV4;11 acute myeloid leukemia (AML) cells
Concentration:

1, 10, 100, 1000 nM
Incubation Time:

4 h
Result:

Reduced S-phase cells to 0.97% in RS4;11 cells and 0.45% in MV4;11 cells.
Increased late apoptotic cells to 75.8% in RS4;11 cells and 62.1% in MV4;11 cells.
Decreased live cells to 17.1% in RS4;11 cells and 23.8% in MV4;11 cells.

Cell Proliferation Assay^[1]

Cell Line:

Panel of p53 wild-type hematologic and solid tumor cell lines, p53 mutant cell lines
Concentration:

0.1, 1, 10, 100, 1000 nM
Incubation Time:

96 h (growth inhibition); 48 h (apoptosis)
Result:

Induced potent growth inhibition (subnanomolar IC₅₀ in multiple lines) and apoptosis in a wide range of p53 wild-type hematologic (AML, T-cell lymphoma, mantle cell lymphoma, diffuse large B-cell lymphoma) and solid tumor (prostate, brain, ovarian, soft tissue sarcoma, neuroblastoma, lung, colorectal) cell lines.
Showed no response in p53 mutant cell lines at concentrations up to 10000 nM.

In Vivo

Seldegamadlin (KT-253) (0.3-3 mg/kg; intravenous injection; single dose, once weekly for 3 weeks) induces sustained tumor regression, complete remission and prolonged survival in RS4;11 acute lymphoblastic leukemia xenografts by degrading MDM2 and activating the p53 pathway^[1].
Seldegamadlin (1-3 mg/kg; intravenous injection; single dose, once weekly for 3 weeks) induces persistent complete remission and prolongs survival in the MV4;11 AML xenograft model by activating the p53 pathway and inducing apoptosis^[1].
Seldegamadlin (1 mg/kg; intravenous injection; Days 0 and 42) induces complete or partial anti-leukemic responses in multiple patient-derived AML xenograft models with systemic disease^[1].
Seldegamadlin (3 mg/kg; intravenous injection; single administration) induces durable complete remission and prolongs survival in the Venetoclax-resistant MOLM-13 acute myeloid leukemia xenograft model^[1].
Seldegamadlin (1 mg/kg; once every 3 weeks; 3 doses total) induces complete remission in 1 of 4 acute myeloid leukemia (AML) patient-derived xenograft models, partial remission in another 2 models, and ultimately achieves significant tumor burden reduction in 3 of the 4 tested models^[1].
Seldegamadlin (1-3 mg/kg; intravenous injection; once every 3 weeks) induces complete remission in a p53 wild-type activated B-cell subtype diffuse large B-cell lymphoma OCI-LY10 xenograft model^[1].
Seldegamadlin (3 mg/kg; intravenous injection; once every 3 weeks) shows no efficacy in p53-mutant activated B-cell subtype diffuse large B-cell lymphoma TMD8 xenografts^[1].
Seldegamadlin (0.3-1 mg/kg; intravenous or intraperitoneal injection; once weekly for 3 weeks, single administration) induces significantly higher expression of p53 target genes (TNFRSF10B, FAS, BBC3) in RS4;11 xenografts under the 1 mg/kg single-administration regimen compared with the exposure-matched 0.3 mg/kg once-weekly regimen for 3 weeks^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

NOD-SCID (female, RS4;11 ALL cells implanted subcutaneously, tumors grown to ~400 mm³)^[1]
Dosage:

0.3, 1, 3 mg/kg
Administration:

i.v.; single dose, once weekly for 3 weeks
Result:

Induced sustained tumor regression and complete responses (3 mg/kg, 1 mg/kg single doses).
Induced transient stable disease (0.3 mg/kg weekly).
Caused MDM2 degradation in tumors.

Animal Model:

Balb/c nude (female, MV4;11 AML cells implanted subcutaneously, tumors grown to ~300 mm³)^[1]
Dosage:

1, 3 mg/kg
Administration:

i.v.; single dose, once weekly for 3 weeks
Result:

Induced complete responses in 5 of 6 animals, with 4 of 6 remaining tumor-free for 6 months (3 mg/kg single dose).
Extended median survival to > 180 days (3 mg/kg single dose).
Induced transient stable disease (1 mg/kg weekly).
Drove robust upregulation of p53 and induction of cleaved caspase-3 in tumors (3 mg/kg single dose).

Animal Model:

NOG (female, sublethally irradiated, injected intravenously with 2×10⁶ primary patient-derived AML blast samples)^[1]
Dosage:

1 mg/kg
Administration:

i.v.; day 0 and day 42
Result:

Achieved complete response with significant reduction in human CD45⁺ tumor burden in peripheral blood and bone marrow, and reduction in hCD34⁺ leukemic blasts in peripheral blood (CTG-2227 model).
Induced partial responses (CTG-2700 and CTG-2240 models).
Showed no response (CTG-2235 model).

Animal Model:

NOD-SCID (female, MOLM-13 AML cells implanted subcutaneously)^[1]
Dosage:

3 mg/kg
Administration:

i.v.；single dose
Result:

Induced transient tumor regression (~7 days) as monotherapy.
Achieved durable complete responses in all 6 animals when combined with Venetoclax.
Extended median survival to > 150 days when combined with 1 week of Venetoclax co-administration.

Animal Model:

Immunocompromised mice^[1]
Dosage:

1 mg/kg
Administration:

every three weeks; 3 doses
Result:

Produced a complete response in the CTG-2227 model.
Produced partial responses in the CTG-2240 and CTG-2700 models.
Showed no response in the CTG-2235 model.

Animal Model:

Immunocompromised mice^[1]
Dosage:

1, 3 mg/kg
Administration:

i.v.; every 3 weeks
Result:

Induced a complete response, with tumor volumes remaining near baseline levels throughout the 35-day observation period.

Animal Model:

Immunocompromised mice^[1]
Dosage:

3 mg/kg
Administration:

i.v.; every 3 weeks
Result:

Showed no efficacy, with tumor volumes progressing similarly to the vehicle control group over the 35-day observation period.

Animal Model:

Immunocompromised mice^[1]
Dosage:

0.3 mg/kg (weekly regimen); 1 mg/kg (single dose)
Administration:

i.v. or i.p.; once weekly; 3 weeks (0.3 mg/kg); i.v. or i.p.; single dose (1 mg/kg)
Result:

Induced robust upregulation of p53 target genes.
Increased TNFRSF10B, FAS, BBC3 mRNA levels.
Induced weaker upregulation of p53 target genes.

Clinical Trial

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS. Nr. 2713618-08-5
Appearance Solid
Molecular Weight 912.87
Formel C₄₈H₅₂Cl₂FN₇O₆
Color White to off-white
SMILES

ClC1=CC2=C([C@]3(C4(CCCCC4)N[C@@H](C(N[C@H]5CC[C@H](C(N6CCC(C7=CC=C8C(N(C)C(N8C9CCC(NC9=O)=O)=O)=C7)CC6)=O)CC5)=O)[C@@H]3C%10=C(F)C(Cl)=CC=C%10)C(N2)=O)C=C1
Synonyms

KT-253
Versand

Room temperature in continental US; may vary elsewhere.
Speicherung

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Publications (1)

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bioRxiv

Ferrous Iron Accumulation Is a Hallmark and Therapeutic Vulnerability of Therapy-Induced Senescence. [Abstract]

2026 May 23:2026.05.20.726695. PMID: 42239384

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 95 mg/mL (104.07 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.0954 mL

5.4772 mL

10.9545 mL

5 mM

0.2191 mL

1.0954 mL

2.1909 mL

10 mM

0.1095 mL

0.5477 mL

1.0954 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (300 KB)
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Chutake YK, et al. KT-253, a Novel MDM2 Degrader and p53 Stabilizer, Has Superior Potency and Efficacy than MDM2 Small-Molecule Inhibitors. Molecular cancer therapeutics. 2025 Apr 02;24(4):497-510. [Content Brief]

[2]. Ji N, et al. Mdm2 degraders and uses thereof. WO2021188948A1. WIPO. 2021-09-23.

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.0954 mL	5.4772 mL	10.9545 mL	27.3862 mL
	5 mM	0.2191 mL	1.0954 mL	2.1909 mL	5.4772 mL
	10 mM	0.1095 mL	0.5477 mL	1.0954 mL	2.7386 mL
	15 mM	0.0730 mL	0.3651 mL	0.7303 mL	1.8257 mL
	20 mM	0.0548 mL	0.2739 mL	0.5477 mL	1.3693 mL
	25 mM	0.0438 mL	0.2191 mL	0.4382 mL	1.0954 mL
	30 mM	0.0365 mL	0.1826 mL	0.3651 mL	0.9129 mL
	40 mM	0.0274 mL	0.1369 mL	0.2739 mL	0.6847 mL
	50 mM	0.0219 mL	0.1095 mL	0.2191 mL	0.5477 mL
	60 mM	0.0183 mL	0.0913 mL	0.1826 mL	0.4564 mL
	80 mM	0.0137 mL	0.0685 mL	0.1369 mL	0.3423 mL
	100 mM	0.0110 mL	0.0548 mL	0.1095 mL	0.2739 mL

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Seldegamadlin

1 Cited Publications

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Seldegamadlin

Publications Citing Use of MedChemExpress (MCE) Seldegamadlin

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