Art. -Nr.: HY-101126

Nuvisertib

Name: Nuvisertib
Brand: MedChemExpress
SKU: HY-101126
Price: 60.00 USD
Availability: InStock
Rating: 5 (4 reviews)

(Synonyms: TP-3654)

4 Cited Publications

Kundenbewertung

Based on 4 publication(s) in Google Scholar

Nuvisertib (TP-3654) is an orally active second-generation pan-PIM kinase inhibitor with K_i values of 5 nM, 239 nM, and 42 nM against PIM-1, PIM-2, and PIM-3, respectively. Nuvisertib inhibits JAK-independent inflammatory and survival signaling pathways, reduces the production of proinflammatory cytokines, restores apoptotic sensitivity, inhibits mTORC1, MYC, and TGF-β signaling pathways, and decreases the expression of fibrosis markers. Nuvisertib selectively impairs the transport function of ABCG2, resensitizes multidrug-resistant cancer cells to cytotoxic drugs, and overcomes JAK2 inhibitor resistance. Nuvisertib can be used in research related to myelofibrosis, renal cell carcinoma, multidrug-resistant cancer, advanced solid tumors, urothelial carcinoma, and prostate adenocarcinoma.

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Reinheit: 99.96%
CAS. Nr.: 1361951-15-6
Formel: C₂₂H₂₅F₃N₄O
Molecular Weight:418.46

Speicherung:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

Nuvisertib Chemical Structure

CAS. Nr.: 1361951-15-6

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- In Vivo
- Clinical Trial
Chemical Information
Publications (4)
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]

PIM1

5 nM (Ki)

PIM2

239 nM (Ki)

PIM3

42 nM (Ki)

JAK2

mTORC1

MYC

TGF-β

ABCG2

Alle Pim Isoform-spezifische Produkte anzeigen :

Alle JAK Isoform-spezifische Produkte anzeigen :

Alle mTOR Isoform-spezifische Produkte anzeigen :

Alle TGF-β Receptor Isoform-spezifische Produkte anzeigen :

In Vitro

Nuvisertib (TP-3654) synergizes with Dordaviprone (HY-15615A) to reduce renal cell carcinoma (RCC) cell viability more potently than either agent alone^[4].
Nuvisertib (2.55-34.33 μM; 72 h) is equally cytotoxic to ABCB1-overexpressing KB-V-1, NCI-ADR-RES, MDR19-HEK293 cells; ABCG2-overexpressing S1-M1-80, H460-MX20, R482-HEK293 cells; and their respective drug-sensitive parental cells, with IC₅₀ values ranging from 2.55 to 34.33 μM^[6].
Nuvisertib (100-500 nM; 72 h) selectively resensitizes ABCG2-overexpressing S1-M1-80, H460-MX20, and R482-HEK293 cells to ABCG2 substrate drugs Topotecan (HY-13768), SN-38 (HY-13704), and Mitoxantrone (HY-13502) in a concentration-dependent manner, with fold-reversal values ranging from 1.2 to 31.9^[6].
Nuvisertib (0-1 μM) selectively inhibits ABCG2-mediated drug efflux in R482-HEK293, S1-M1-80, and H460-MX20 cells with IC₅₀ values of 140 nM, 240 nM, and 200 nM, respectively, and does not affect ABCB1-mediated drug efflux^[6].
Nuvisertib (0.1-0.5 μM; 72 h) does not affect ABCG2 protein expression in ABCG2-overexpressing S1-M1-80 or H460-MX20 cancer cells when incubated at concentrations from 0.1 to 0.5 μM for 72 h^[6].
Nuvisertib binds to the substrate-binding pocket of human ABCG2 (PDB: 6VXH) with a binding energy of -58.23 kcal/mol, forming hydrophobic interactions and one hydrogen bond with specific amino acid residues^[6].
Nuvisertib (0.03-3 μM; 12 h) dose-dependently reduces phospho-BAD^S112 levels in UM-UC-3 bladder cancer cells without altering phospho-4EBP1^Th37/46 levels^[7].
Nuvisertib (0.01-100 μM; 6 or 10 days) inhibits colony formation in T24 and UM-UC-3 bladder cancer cells, with average EC₅₀ values of 1.1 μM and 2.2 μM, respectively^[7].
Nuvisertib significantly inhibits colony growth of human MPN/MF CD34⁺ hematopoietic progenitor cells^[8].
Nuvisertib (0.5 μM; 48 h) enhances Topotecan-induced apoptosis in ABCG2-overexpressing S1-M1-80 colon cancer cells, increasing total apoptosis from approximately 4% to 23%, without inducing apoptosis on its own^[6].
Nuvisertib (0.25-1.0 μM) potently reduces proliferation and induces apoptosis in JAK2^V617F- or MPL^W515L-expressing hematopoietic cells (including Ruxolitinib (HY-50856)-resistant cells), while having only modest effects on wild-type JAK2-expressing Ba/F3-EpoR cells^[8].
Nuvisertib (10 μM starting concentration with three-fold serial dilutions; up to 120 minutes) potently inhibits purified PIM-1, PIM-2, and PIM-3 kinases with K_i values of 5 nM, 239 nM, and 42 nM, respectively, and exhibits at least 10-fold selectivity for PIM-1 over other tested kinases^[7].
Nuvisertib (30 μM starting concentration with three-fold serial dilutions) does not inhibit hERG potassium channels in CHO cells stably expressing hERG, with an IC₅₀ greater than 30 μM^[7].
Nuvisertib (0.1 nM‑100 μM) potently inhibits PIM-1-mediated BAD phosphorylation at serine 112 in transfected HEK-293 cells, with an average EC₅₀ of 67 nM^[7].

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

Cell Cytotoxicity Assay^[6]

Cell Line:

KB-3-1, KB-V-1, OVCAR-8, NCI-ADR-RES, S1, S1-M1-80, H460, H460-MX20, pcDNA3.1-HEK293, MDR19-HEK293, R482-HEK293
Concentration:

2.55-34.33 μM
Incubation Time:

72 h
Result:

Exhibited similar cytotoxicity in drug-sensitive parental cells and their ABCB1- or ABCG2-overexpressing multidrug-resistant variants, with IC₅₀ values ranging from 2.55 μM to 34.33 μM.

Cell Cytotoxicity Assay^[6]

Cell Line:

S1-M1-80, H460-MX20, R482-HEK293, S1, H460, pcDNA3.1-HEK293
Concentration:

100-500 nM
Incubation Time:

72 h
Result:

Resensitized ABCG2-overexpressing cells to ABCG2 substrate drugs in a concentration-dependent manner.
Achieved fold-reversal values of 2.1-3.9 for Topotecan, 2.6-5.9 for SN-38, and 3.3-27.0 for Mitoxantrone in S1-M1-80 cells.
Achieved fold-reversal values of 4.6-19.9 for Topotecan, 8.8-31.9 for SN-38, and 1.2-6.5 for Mitoxantrone in H460-MX20 cells.
Achieved fold-reversal values of 2.9-8.8 for Topotecan, 3.3-7.0 for SN-38, and 2.5-6.0 for Mitoxantrone in R482-HEK293 cells.

Apoptosis Analysis^[6]

Cell Line:

S1, S1-M1-80
Concentration:

0.5 μM (alone or in combination with 5 μM Topotecan)
Incubation Time:

48 h
Result:

Did not induce significant apoptosis in either S1 or S1-M1-80 cells when used alone.
Increased total apoptosis in S1-M1-80 cells from approximately 4% to 23% when combined with Topotecan.

Western Blot Analysis^[6]

Cell Line:

S1-M1-80, H460-MX20
Concentration:

0.1-0.5 μM
Incubation Time:

72 h
Result:

Did not significantly alter the protein expression of ABCG2 in either S1-M1-80 or H460-MX20 cells at any tested concentration.

Western Blot Analysis^[7]

Cell Line:

UM-UC-3 bladder cancer cells
Concentration:

0.03 μM; 0.3 μM; 1 μM; 3 μM
Incubation Time:

12 h
Result:

Dose-dependently reduced levels of phospho-BAD (S112) without causing appreciable changes in phospho-4EBP1 (Th37/46) levels.

In Vivo

Nuvisertib (150 mg/kg; p.o.; once daily; 6 weeks) (TP-3654) reduces leukocytosis, splenomegaly, and bone marrow fibrosis in Jak2^V617F-induced myelofibrosis in C57BL/6 mice^[5].
Nuvisertib (150 mg/kg; p.o.; once daily; 12 weeks) preferentially inhibits Jak2^V617F mutant hematopoietic progenitors, reducing leukocytosis and thrombocytosis in chimeric C57BL/6 mice with myelofibrosis^[5].
Nuvisertib (150 mg/kg; p.o.; once daily; 3 weeks) reduces leukocytosis, splenomegaly, and bone marrow fibrosis, and improves survival in MPL^W515L-induced myelofibrosis in BALB/c mice^[5].
Nuvisertib (25 mg/kg; i.p.; 5 days on, 2 days off; 3 weeks) inhibits PIM-1-driven prostate adenocarcinoma xenograft growth in female Nu/Nu mice^[7].
Nuvisertib (25 mg/kg; i.p.; 5 days on, 2 days off; 3 weeks) inhibits PIM-2-driven fibrosarcoma xenograft growth in female Nu/Nu mice^[7].
Nuvisertib (200 mg/kg; p.o.; 5 days on, 2 days off; 3 weeks) inhibits bladder carcinoma xenograft growth in female Nu/Nu mice^[7].
Nuvisertib (200 mg/kg; p.o.; 5 days on, 2 days off; 3 weeks) inhibits prostate adenocarcinoma xenograft growth in male Nu/Nu mice^[7].

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

Animal Model:

C57BL/6 (lethally irradiated; transplanted with BM cells from pI-pC induced Mx1Cre; Jak2VF/VF mice; treatment started 6 weeks post-transplant)^[5]
Dosage:

150 mg/kg
Administration:

p.o.; once daily; 6 weeks
Result:

Significantly reduced white blood cell (WBC) and neutrophil counts.
Significantly reduced myeloid (Gr-1+/Mac-1+) cells in bone marrow (BM) and spleens.
Significantly reduced LSK, LK, and GMP populations in BM and spleens.
Significantly reduced CFU-GM colonies in BM.
Significantly reduced spleen size/weight.
Significantly attenuated BM fibrosis.

Animal Model:

C57BL/6 (lethally irradiated; transplanted with 1:1 mixed BM cells from Mx1Cre; Jak2VF/VF GFP+ mice and WT C57BL/6 mice; treatment started 6 weeks post-transplant)^[5]
Dosage:

150 mg/kg
Administration:

p.o.; once daily; 12 weeks
Result:

Significantly reduced WBC, neutrophil, and platelet counts.
Significantly reduced percentage of Jak2V617F mutant GFP+ LSK, LK, myeloid (Gr-1+), and megakaryocytic (CD41+) cells in BM.

Animal Model:

BALB/c (lethally irradiated; transplanted with WT BALB/c BM cells transduced with MPLW515L-expressing retrovirus; treatment started 3 weeks post-transplant)^[5]
Dosage:

150 mg/kg
Administration:

p.o.; once daily; 3 weeks
Result:

Significantly reduced WBC and neutrophil counts.
Significantly reduced myeloid precursors (Gr-1+/Mac-1+) in BM and spleens.
Significantly increased survival.
Significantly reduced splenomegaly.
Significantly reduced BM fibrosis.

Animal Model:

Nu/Nu (female; prostate adenocarcinoma xenograft model)^[7]
Dosage:

25 mg/kg
Administration:

i.p.; 5 days on, 2 days off; 3 weeks
Result:

Significantly reduced tumor growth compared to vehicle-treated mice.
Showed no significant changes in body weight.

Animal Model:

Nu/Nu (female; fibrosarcoma xenograft model)^[7]
Dosage:

25 mg/kg
Administration:

i.p.; 5 days on, 2 days off; 3 weeks
Result:

Significantly reduced tumor growth compared to vehicle-treated mice.
Showed no significant changes in body weight.

Animal Model:

Nu/Nu (female; bladder carcinoma xenograft model)^[7]
Dosage:

200 mg/kg
Administration:

p.o.; 5 days on, 2 days off; 3 weeks
Result:

Significantly reduced tumor volume and final tumor weight compared to vehicle-treated mice.
Showed no significant changes in body weight or gross adverse toxicity.

Animal Model:

Nu/Nu (male; prostate adenocarcinoma xenograft model)^[7]
Dosage:

200 mg/kg
Administration:

p.o.; 5 days on, 2 days off; 3 weeks
Result:

Significantly reduced tumor volume and final tumor weight compared to vehicle-treated mice.
Showed no significant changes in body weight or gross adverse toxicity.

Clinical Trial

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

Chemical Information

CAS. Nr. 1361951-15-6
Appearance Solid
Molecular Weight 418.46
Formel C₂₂H₂₅F₃N₄O
Color White to light yellow
SMILES

OC(C)(C)[C@H]1CC[C@H](NC2=NN3C(C=C2)=NC=C3C4=CC=CC(C(F)(F)F)=C4)CC1
Synonyms

TP-3654
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (4)

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Journal Impact Factor

Arterioscler Thromb Vasc Biol

PIM1 (Moloney Murine Leukemia Provirus Integration Site) Inhibition Decreases the Nonhomologous End-Joining DNA Damage Repair Signaling Pathway in Pulmonary Hypertension. [Abstract]

2020 Mar;40(3):783-801. PMID: 31969012
Cancer Res Commun

Pim kinase inhibitors increase gilteritinib cytotoxicity in FLT3-ITD acute myeloid leukemia through GSK-3β activation and c-Myc and Mcl-1 proteasomal degradation. [Abstract]

2024 Feb 16;4(2):431-445. PMID: 38284896
Biochem Biophys Res Commun

β-catenin stimulates Tcf7l1 degradation through recruitment of casein kinase 2 in mouse embryonic stem cells. [Abstract]

2020 Apr 2;524(2):280-287. PMID: 31987502

Nuvisertib purchased from MedChemExpress. Usage Cited in: Biochem Biophys Res Commun. 2020 Apr 2;524(2):280-287. [Abstract]

Western blot analysis of Tcf7l1 protein levels in mESCs pre-treated with the indicative different small molecules for 1 h and then treated with CHIR for 24 h.
bioRxiv

Radiation synergizes with BET inhibition to stimulate durable, systemic anti-tumor immunity in murine cancer models. [Abstract]

2026 Feb 18:2026.02.16.706212. PMID: 41757027

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 50 mg/mL (119.49 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

2.3897 mL

11.9486 mL

23.8971 mL

5 mM

0.4779 mL

2.3897 mL

4.7794 mL

10 mM

0.2390 mL

1.1949 mL

2.3897 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, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

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)}

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: 2.5 mg/mL (5.97 mM); Suspended solution; Need ultrasonic

This protocol yields a suspended solution of 2.5 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 2

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.08 mg/mL (4.97 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.08 mg/mL (4.97 mM); Clear solution

This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (303 KB)
SDS (643 KB)
- English - EN (643 KB)
- Français - FR (643 KB)
- Deutsch - DE (643 KB)
- Norwegian - NO (643 KB)
- Español - ES (643 KB)
- Swedish - SV (643 KB)
- Italian - IT (643 KB)
- Korean - KR (643 KB)
- Portuguese - PT (643 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]. Abruzzese E, et al. The Path Forward in MF: Small Molecules in the Limelight. Cancers (Basel). 2026 Apr 25;18(9):1370.

[2]. El Chaer F, et al. Nuvisertib (TP-3654), an investigational selective PIM1 kinase inhibitor, showed durable clinical response and sustained hematological improvement in relapsed/refractory myelofibrosis patients. Blood. 2024;144(Suppl 1):655.

[3]. Mascarenhas J, et al. Preliminary data from the Phase I/II study of nuvisertib, an oral investigational selective PIM1 inhibitor, in combination with momelotinib showed clinical responses in patients with relapsed/refractory myelofibrosis. Blood. 2025;146(Suppl 1):482. Abstract 634A.

[4]. Meza KS, et al. Abstract 3174: Nuvisertib (TP‑3654) and Dordaviprone (ONC201) synergize to reduce renal cell carcinoma cell viability. Cancer Res. 2026;86(7_Supplement):3174.

[5]. Dutta A, et al. Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models. Leukemia. 2022 Mar;36(3):746-759.

[6]. Wu CP, et al. The Second-Generation PIM Kinase Inhibitor TP-3654 Resensitizes ABCG2-Overexpressing Multidrug-Resistant Cancer Cells to Cytotoxic Anticancer Drugs. International journal of molecular sciences. 2021 Aug 30;22(17):9440.

[7]. Foulks JM, et al. A small-molecule inhibitor of PIM kinases as a potential treatment for urothelial carcinomas. Neoplasia. 2014 May;16(5):403-12. [Content Brief]

[8]. Nath D, et al. The PIM Kinase Inhibitor TP‑3654 in Combination with Ruxolitinib Exhibits Marked Improvement of Myelofibrosis in Murine Models. Blood. 2018;132(Suppl 1):54. Abstract 635.

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

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.3897 mL	11.9486 mL	23.8971 mL	59.7429 mL
	5 mM	0.4779 mL	2.3897 mL	4.7794 mL	11.9486 mL
	10 mM	0.2390 mL	1.1949 mL	2.3897 mL	5.9743 mL
	15 mM	0.1593 mL	0.7966 mL	1.5931 mL	3.9829 mL
	20 mM	0.1195 mL	0.5974 mL	1.1949 mL	2.9871 mL
	25 mM	0.0956 mL	0.4779 mL	0.9559 mL	2.3897 mL
	30 mM	0.0797 mL	0.3983 mL	0.7966 mL	1.9914 mL
	40 mM	0.0597 mL	0.2987 mL	0.5974 mL	1.4936 mL
	50 mM	0.0478 mL	0.2390 mL	0.4779 mL	1.1949 mL
	60 mM	0.0398 mL	0.1991 mL	0.3983 mL	0.9957 mL
	80 mM	0.0299 mL	0.1494 mL	0.2987 mL	0.7468 mL
	100 mM	0.0239 mL	0.1195 mL	0.2390 mL	0.5974 mL

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Nuvisertib

4 Cited Publications

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Nuvisertib

Publications Citing Use of MedChemExpress (MCE) Nuvisertib

Alle Pim Isoform-spezifische Produkte anzeigen

Alle JAK Isoform-spezifische Produkte anzeigen

Alle mTOR Isoform-spezifische Produkte anzeigen

Alle TGF-β Receptor Isoform-spezifische Produkte anzeigen