Cat. No.: HY-108697

PT2399

Name: PT2399
Brand: MedChemExpress
SKU: HY-108697
Price: 300.00 USD
Availability: InStock
Rating: 5 (13 reviews)

13 Cited Publications

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Based on 13 publication(s) in Google Scholar

PT2399 is a selective and orally active HIF-2α antagonist (IC₅₀ < 5 nM) that binds the PAS-B domain and disrupts HIF-2α-ARNT heterodimerization. PT2399 inhibits HIF-2α-driven transcription, destabilizes HIF-2α, and suppresses HIF target genes without inhibiting HIF1α. PT2399 reduces tumor cell proliferation, vessel area, circulating tumor-derived VEGFA/VEGF, and lactate while increasing pyruvate. PT2399 can be used for research on clear cell renal cell carcinoma and chronic myeloid leukemia (CML).

For research use only. We do not sell to patients.

Purity : 99.96%
CAS No.: 1672662-14-4
Formula: C₁₇H₁₀F₅NO₄S
Molecular Weight:419.32

Storage:

-20°C, stored under nitrogen

* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

PT2399 Chemical Structure

CAS No.: 1672662-14-4

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Top Publications Citing

Use of MCE Products

Fluorescent Dye

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

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Publications (13)
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[1]

HIF-2α

< 5 nM (IC₅₀)

HIF-2α

6 nM (EC₅₀)

All HIF/HIF Prolyl-Hydroxylase Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
786-0	EC50	0.006 μM	Inhibition of HIF-2α-driven HRE-dependent luciferase reporter activity in 786-O ccRCC cells. Inhibition of HIF-2α-driven HRE-dependent luciferase reporter activity in 786-O ccRCC cells.	30289716
786-0	EC50	14 nM	Inhibition of VEGFA secretion in 786-O ccRCC cells. Inhibition of VEGFA secretion in 786-O ccRCC cells.	30289716
786-0	EC50	233 nM	Free-fraction adjusted inhibition of VEGFA secretion in 786-O ccRCC cells. Free-fraction adjusted inhibition of VEGFA secretion in 786-O ccRCC cells.	30289716

In Vitro

Anti-cancerApoptosisCarbohydrate MetabolismCell Cycle RegulationLocal Vascular RegulationOthers

Anti-cancer

PT2399 (compound 10f) inhibits HIF-2α-driven HRE luciferase activity in 786-O cells with an EC₅₀ of 6 nM^[1].
PT2399 (0.02-2 µM) disrupts HIF2α-ARNT1 interaction in 786-O, A498, UMRC-2, 769-P, and RCC10 cells^[4].
PT2399 (2 µM; 16 h) accelerates HIF2α protein decay in 786-O cells, reducing half-life from 63.66 to 19.77 min^[4].
PT2399 (0.02-200 µM; 16 h) inhibits HIF-responsive luciferase activity in 786-O VHL^−/− cells without affecting constitutive luciferase reporters^[4].
PT2399 (0.2-2 µM; 21 d) inhibits soft agar growth of 786-O and A498 cells, while UMRC-2, 769-P, SKRC-20, UMRC-6, RCC10, and SLR21 cells are insensitive^[4].
PT2399 (0.2-20 µM; up to 14-18 d) has minimal antiproliferative effect in 786-O cells at 0.2 and 2 µM, whereas 20 µM causes HIF2α-independent growth inhibition^[4].
PT2399 (0.02-20 µM for HRE-Luc; 0.2-2 µM for soft agar) inhibits HIF-responsive luciferase activity in UMRC-2 cells independently of HIF1α, while UMRC-2 soft agar growth remains insensitive^[4].
PT2399 inhibits HIF-2α protein expression in K562 and MEG-01 CML cells^[5].
PT2399 (0-72 h) suppresses proliferation of K562 and MEG-01 CML cells over 72 h, and PT2399 combined with TKI further reduces proliferation^[5].
PT2399 (20-40 μM; 0-72 h) inhibits proliferation of primary CML cells, with 40 μM more effective than 20 μM at later time points^[5].
PT2399 (7 days) reduces colony formation by primary CML cells^[5].

Anti-cancer

Apoptosis

PT2399 increases Annexin V+ apoptosis in primary CML cells^[5].

Anti-cancer

Carbohydrate Metabolism

PT2399 shifts K562 metabolism away from glycolysis, decreasing lactate and increasing pyruvate^[5].

Anti-cancer

Cell Cycle Regulation

PT2399 (0.2-20 µM; 24-48 h) represses HIF2α-dependent transcriptional output and HIF2α protein in 786-O cells without suppressing the HIF1α-specific target BNIP3^[4].
PT2399 (0.2-2 µM) mediates HIF target repression in M2A cells, with HIF2α S304M conferring partial resistance^[4].
PT2399 (0.2-2 µM; 24 h) variably suppresses HIF target mRNAs across ccRCC lines, with the strongest repression in 786-O and A498 cells^[4].

Anti-cancer

Local Vascular Regulation

PT2399 inhibits VEGFA secretion in 786-O cells with EC₅₀ 14 nM^[1].
PT2399 lowers VEGFα secretion by K562 and MEG-01 CML cells^[5].
PT2399 impairs K562-driven HUVEC tube formation^[5].

Cell Cycle Regulation

PT2399 (0.2-2 µM; 21 d) suppresses HIF target genes and soft agar growth in 786-O cells through on-target HIF2α inhibition^[4].

Others

PT2399 binds HIF-2α PAS-B with SPA IC₅₀ <0.005 μM^[1].
PT2399 (10 µM; 5 h) failed to dissociate HIF-2 dimers in HEK293T cells expressing HIF-2α G323E and/or HIF-1β F446L^[3].
PT2399 has minimal activity across a 68-target receptor/ion-channel/enzyme panel^[4].

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

Western Blot Analysis^[3]

Cell Line:

HEK293T cells
Concentration:

10 µM
Incubation Time:

5 h
Result:

HIF-2 dimers were preserved in cells expressing HIF-2α G323E and/or HIF-1β F446L.
Both mutants were sufficient to preserve HIF-2 dimers, and the effects appeared additive.
At 10 µM for 5 h, HIF-2 dimers were not dissociated when HIF-2α G323E and/or HIF-1β F446L were expressed.

Real Time qPCR^[4]

Cell Line:

786-O VHL−/− ccRCC cells
Concentration:

0.2, 2, and 20 µM
Incubation Time:

24 and 48 h
Result:

Repressed NDRG1, VEGF, Cyclin D1, and GLUT1 mRNAs and reduced HIF2α protein and secreted VEGF; the HIF1α-specific target BNIP3 was not suppressed.
Microarray analysis showed overlap with HIF2α sgRNA effects and downregulation of hypoxia-, HIF-, and c-Myc-induced gene sets, with GSEA NES values of 2.95, 2.39, 3.01, and 2.21 for representative sets.

Western Blot Analysis^[4]

Cell Line:

786-O cells
Concentration:

2 µM
Incubation Time:

16 h; 0, 0.5, 1, 2, 3, 5, and 7 h (cycloheximide chase)
Result:

HIF2α half-life decreased from 63.66 min in DMSO-treated cells to 19.77 min under HIF2α inhibition.

Real Time qPCR^[4]

Cell Line:

786-O HIF2α−/− cells reconstituted with empty vector, HIF2α WT, or HIF2α S304M
Concentration:

0.2 and 2 µM
Incubation Time:

21 days (soft agar)
Result:

Repressed NDRG1, VEGF, Cyclin D1, and GLUT1 in HIF2α WT-reconstituted cells but not in empty-vector or HIF2α S304M cells.
Reduced soft agar colony formation in HIF2α WT cells, and this effect was reversed by HIF2α S304M; HIF2α−/− cells did not form colonies unless rescued with HIF2α.

Cell Proliferation Assay^[4]

Cell Line:

786-O, A498, UMRC-2, 769-P, RCC10, SKRC-20, UMRC-6, and SLR21 renal carcinoma cells
Concentration:

0.2 and 2 µM
Incubation Time:

21 days
Result:

Inhibited soft agar colony formation in 786-O and A498 cells.
UMRC-2, 769-P, SKRC-20, UMRC-6, and SLR21 cells were insensitive; RCC10 soft agar growth was also unaffected despite suppression by HIF2α sgRNA.

Real Time qPCR^[4]

Cell Line:

ccRCC cell panel including 786-O, A498, UMRC-2, 769-P, RCC10, SKRC-20, UMRC-6, Caki-2, M1A, M2A, and SLR21, plus pVHL-isogenic 786-O, A498, UMRC-2, and 769-P cells
Concentration:

0.2 and 2 µM
Incubation Time:

24 h (RCC10)
Result:

786-O and A498 cells showed the greatest repression of HIF target genes, whereas UMRC-2 and 769-P cells showed weaker repression; the panel showed variable suppression of VEGF, Cyclin D1, and GLUT1.

Parmacokinetics

Species	Dose	Route	AUC_0-t	T_1/2	F	CL	V_ss
Mice^[1]	10 mg/kg	p.o.	7.3 μM·h	7.3 h	67 %	/	/
Mice^[1]	3 mg/kg	i.v.	/	/	/	34.3 mL/min/kg	7.4 L/kg

In Vivo

Anti-cancerApoptosisLocal Vascular RegulationCell Cycle Regulation

Anti-cancer

PT2399 (10 mg/kg; p.o.; twice daily; 21 days) causes rapid regression of established 786-O ccRCC xenograft tumors in mice^[1].
PT2399 (100 mg/kg; p.o. by oral gavage; every 12 h; typically 4 weeks) inhibited renal cell carcinoma tumorgraft growth in NOD/SCID mice, with 60% overall growth inhibition^[3].
PT2399 (30-100 mg/kg; once daily) inhibits VHL^−/− ccRCC patient-derived xenograft (PDX) growth^[4].
PT2399 (100 mg/kg; p.o. (oral gavage); once daily; 14 days) alone modestly suppresses CML progression in mice^[5].
PT2399 (100 mg/kg; p.o. (oral gavage); once daily; 14 days) extends survival and improves TKI efficacy in K562 CDX mice^[5].
PT2399 (100 mg/kg; p.o. (oral gavage); once daily; 14 days) extends survival in cell-derived xenograft (CDX) CML model
in B-NDG mice^[5].

Anti-cancer

Apoptosis

Local Vascular Regulation

PT2399 (30 mg/kg; twice daily; 2 days) produces on-target HIF2α inhibition and pharmacodynamic responses in 786-O orthotopic ccRCC tumors^[4].

Anti-cancer

Cell Cycle Regulation

PT2399 (30 mg/kg; twice daily; 1 month) does not suppress UMRC-2 orthotopic tumor growth despite suppressing NDRG1 and Cyclin D1 mRNAs^[4].

Anti-cancer

Cell Cycle Regulation

Local Vascular Regulation

PT2399 (10 mg/kg; p.o.; twice daily; 3 days) suppresses HIF-2α-driven tumor gene expression and circulating tumor-derived VEGFA in 786-O ccRCC xenografts^[1].

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

Animal Model:

Female SCID/beige mice injected with 786-O cells^[1]
Dosage:

10 mg/kg
Administration:

p.o.; twice daily; 3 days
Result:

Inhibited HIF-2α-driven VEGFA and CCND1 transcription in tumor and completely abolished circulating human tumor-derived VEGFA.

Animal Model:

Female SCID/beige mice injected with 786-O cells^[1]
Dosage:

10 mg/kg
Administration:

p.o.; twice daily; 21 days
Result:

Produced rapid regression of established 786-O xenograft tumors.

Animal Model:

nude mice^[4]
Dosage:

30 mg/kg
Administration:

twice daily; 2 days
Result:

After two days, the 3XHRE-Luc signal decreased by more than 60%; CMV-Luc tumors were not decreased.
The 3XHRE-Luc signal recovered after washout and decreased again after rechallenge.
HIF-responsive mRNAs decreased, Ki-67 staining decreased, Caspase 3 cleavage increased, and microvessel density decreased.

Animal Model:

nude mice^[4]
Dosage:

30 mg/kg
Administration:

twice daily; 1 month
Result:

Orthotopic UMRC-2 tumor growth was not suppressed; relative bioluminescence signal showed no suppression.
In UMRC-2 orthotopic tumors, NDRG1 and Cyclin D1 mRNAs were suppressed despite no growth inhibition.

Animal Model:

C57BL/6 (male and female, 6-8 weeks old)^[5]
Dosage:

100 mg/kg
Administration:

p.o. (oral gavage); once daily; 14 days
Result:

Slightly suppressed CML onset.
Reduced GFP+ leukemia cells in peripheral blood and prolonged survival compared with TKI alone.

Animal Model:

B-NDG (NOD.CB17-PrkdcscidIl2rgtm1/Bcgen; male and female, 6-8 weeks old)^[5]
Dosage:

100 mg/kg
Administration:

p.o. (oral gavage); once daily; 14 days
Result:

Extended survival.
Further extended survival compared with TKI alone in K562 CDX mice.

Animal Model:

B-NDG (NOD.CB17-PrkdcscidIl2rgtm1/Bcgen; male and female, 6-8 weeks old)^[5]
Dosage:

100 mg/kg
Administration:

p.o. (oral gavage); once daily; 14 days
Result:

Extended survival.
Further extended survival compared with TKI alone in MEG-01 CDX mice.

Related Protocols :

Chemical Information

CAS No. 1672662-14-4
Appearance Solid
Molecular Weight 419.32
Formula C₁₇H₁₀F₅NO₄S
Color White to off-white
SMILES

N#CC1=CC(F)=CC(OC2=CC=C(S(=O)(C(F)F)=O)C3=C2CC(F)(F)[C@H]3O)=C1
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

-20°C, stored under nitrogen

* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

Publications (13)

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Journal Impact Factor

Cancer Discov

HIF-2-dependent Regulation of PTHrP and Paraneoplastic Hypercalcemia in Aggressive Clear Cell Renal Cell Carcinoma. [Abstract]

2025 Oct 9. PMID: 41065553
Nat Commun

Human iPSC-based Modeling of Pulmonary Fibrosis Reveals p300/CBP Inhibition Suppresses Alveolar Transitional Cell State. [Abstract]

2026 Feb 12;17(1):1214. PMID: 41680175
Nat Commun

BMAL1 and ARNT enable circadian HIF2α responses in clear cell renal cell carcinoma. [Abstract]

2025 Jul 1;16(1):5834. PMID: 40595592
EMBO J

A mitochondrial EglN1-AMPKα axis drives breast cancer progression by enhancing metabolic adaptation to hypoxic stress. [Abstract]

2023 Oct 16;42(20):e113743. PMID: 37661833
Cell Prolif

Hypoxia Exacerbates Periapical Periodontitis-Associated Pathological Bone Loss via the Hypoxia-Inducible Factor-2α-Calmodulin-Dependent Protein Kinase IV Axis. [Abstract]

2025 Dec 30:e70160. PMID: 41467319
J Biol Eng

Poly-3-hydroxybutyrate-co-3-hydroxyvalerate(PHBV)-Polyethylene glycol 20k(PEG20k) as a promising delivery system for PT2399 in the treatment of disc degeneration. [Abstract]

2024 Jan 22;18(1):11. PMID: 38254196
Stem Cell Reports

2026 Aug 11;21(8):103008. PMID: 42425087
FASEB J

SGLT2 inhibitor dapagliflozin attenuates cardiac fibrosis and inflammation by reverting the HIF-2α signaling pathway in arrhythmogenic cardiomyopathy. [Abstract]

2022 Jul;36(7):e22410. PMID: 35713937
Hum Mol Genet

Continuous, but not intermittent, regimens of hypoxia prevent and reverse ataxia in a murine model of Friedreich's ataxia. [Abstract]

2023 Aug 7;32(16):2600-2610. PMID: 37260376
bioRxiv

2026 Jul 3:2026.06.30.734089. PMID: 42427540
Blood Red Cells Iron

2026 Mar 9.
the Scripps Research Institute

2025.
Biomed Pharmacother

The HIF-2α/PPARα pathway is essential for liraglutide-alleviated, lipid-induced hepatic steatosis. [Abstract]

2021 Aug:140:111778. PMID: 34062416

Solvent & Solubility

In Vitro:

DMSO : ≥ 200 mg/mL (476.96 mM; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

* "≥" means soluble, but saturation unknown.

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

2.3848 mL

11.9241 mL

23.8481 mL

5 mM

0.4770 mL

2.3848 mL

4.7696 mL

10 mM

0.2385 mL

1.1924 mL

2.3848 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 (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molarity Calculator

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

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Dilution Calculator

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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 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 1.67 mg/mL (3.98 mM); Clear solution

This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 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 2

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

Solubility: ≥ 1.67 mg/mL (3.98 mM); Clear solution

This protocol yields a clear solution of ≥ 1.67 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (16.7 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

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

Solubility: ≥ 1.67 mg/mL (3.98 mM); Clear solution

This protocol yields a clear solution of ≥ 1.67 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 (16.7 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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mg/kg
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g
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μL
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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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (310 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)

References

[1]. Wehn PM, et al. Design and Activity of Specific Hypoxia-Inducible Factor-2α (HIF-2α) Inhibitors for the Treatment of Clear Cell Renal Cell Carcinoma: Discovery of Clinical Candidate ( S)-3-((2,2-Difluoro-1-hydroxy-7-(methylsulfonyl)-2,3-dihydro-1 H-inden-4-yl)oxy)-5-fluorobenzonitrile (PT2385). J Med Chem. 2018 Nov 8;61(21):9691-9721. [Content Brief]

[2]. Sun DR, et al. Exploring the inhibition mechanism on HIF-2 by inhibitor PT2399 and 0X3 using molecular dynamics simulations. J Mol Recognit. 2018 Oct;31(10):e2730.

[3]. Chen W, et al. Targeting renal cell carcinoma with a HIF-2 antagonist. Nature. 2016 Nov 03;539(7627):112-117. [Content Brief]

[4]. Cho H, et al. On-target efficacy of a HIF-2α antagonist in preclinical kidney cancer models. Nature. 2016 Nov 03;539(7627):107-111. [Content Brief]

[5]. Wang J, et al. HIF-2α inhibition disrupts leukemia stem cell metabolism and impairs vascular microenvironment to enhance chronic myeloid leukemia treatment. Cancer letters. 2024 Aug 10;597:217060.

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	2.3848 mL	11.9241 mL	23.8481 mL	59.6203 mL
	5 mM	0.4770 mL	2.3848 mL	4.7696 mL	11.9241 mL
	10 mM	0.2385 mL	1.1924 mL	2.3848 mL	5.9620 mL
	15 mM	0.1590 mL	0.7949 mL	1.5899 mL	3.9747 mL
	20 mM	0.1192 mL	0.5962 mL	1.1924 mL	2.9810 mL
	25 mM	0.0954 mL	0.4770 mL	0.9539 mL	2.3848 mL
	30 mM	0.0795 mL	0.3975 mL	0.7949 mL	1.9873 mL
	40 mM	0.0596 mL	0.2981 mL	0.5962 mL	1.4905 mL
	50 mM	0.0477 mL	0.2385 mL	0.4770 mL	1.1924 mL
	60 mM	0.0397 mL	0.1987 mL	0.3975 mL	0.9937 mL
	80 mM	0.0298 mL	0.1491 mL	0.2981 mL	0.7453 mL
	100 mM	0.0238 mL	0.1192 mL	0.2385 mL	0.5962 mL

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PT2399

Publications Citing Use of MedChemExpress (MCE) PT2399

All HIF/HIF Prolyl-Hydroxylase Isoforms