Perfluoroundecanoic acid

Cat. No.: HY-W142432 Purity: 99.85%: Data Sheet
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Perfluoroundecanoic acid is a perfluoroalkyl substance (PFAS). Perfluoroundecanoic acid is an orally active oxidative stress inducer. Perfluoroundecanoic acid promotes macrophage M2 polarization, activates Wnt/β-catenin signaling and enhances β-catenin nuclear accumulation. Perfluoroundecanoic acid -induced M2 phenotype macrophage accelerates tumor progression in vitro and in vivo. Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice. Perfluoroundecanoic acid inhibits Leydig cell development in pubertal male rats via inducing oxidative stress and autophagy. Perfluoroundecanoic acid accelerates insulitis development in a mouse model of type 1 diabetes. Perfluoroundecanoic acid can be used for the study of ovarian cancer, type 1 diabetes and inflammation.

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

Perfluoroundecanoic acid Chemical Structure

CAS No. : 2058-94-8

Size	Stock	Quantity
500 mg	In-stock	Estimated Time of Arrival: December 31
1 g	In-stock	Estimated Time of Arrival: December 31
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Other Forms of Perfluoroundecanoic acid:

Perfluoroundecanoic acid (Standard) Get quote

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Biological Activity
Purity & Documentation
References
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Description

In Vitro

Perfluoroundecanoic acid (2-16 μM, 24 h) promotes M2 polarization of RAW264.7 macrophages by increasing the protein and mRNA levels of M2 markers (ARG1, CD163, TGF-β) and decreasing M1 marker (iNOS)^[1].
Perfluoroundecanoic acid (8 μM, 24 h) activates Wnt/β-catenin signaling in RAW264.7 cells, enhancing β-catenin expression and nuclear translocation^[1].
Perfluoroundecanoic acid (8 μM, 24 h)-pretreated RAW264.7 cell conditioned medium promotes migration and invasion of A2780 and SKOV3 ovarian cancer cells, which is reversed by β-catenin inhibitor ICG001 (HY-14428)^[1].

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

Western Blot Analysis^[1]

Cell Line:	RAW264.7 cells
Concentration:	2, 4, 8, 16 μM
Incubation Time:	24 h
Result:	Increased protein levels of M2 markers (ARG1, CD163) and decreased M1 marker (iNOS), with the most significant changes at 8 μM. Increased β-catenin protein level and nuclear translocation; no significant changes in p-smad2, p-smad3, p-Akt, p-mTOR, or PPARα.

In Vivo

Perfluoroundecanoic acid (8 μM pretreated RAW264.7 cells, co-injected intraperitoneally with SKOV3 cells for 4 weeks) increases the number and weight of ovarian cancer metastatic nodules in BALB/c nude mice^[1].
Perfluoroundecanoic acid (0-10 mg/kg, p.o., daily, 21-35 days) inhibits Leydig cell development and function via oxidative stress and autophagy in pubertal male Sprague-Dawley rats^[2].
Perfluoroundecanoic acid (3-300 μg/L in drinking water, from mating through gestation, lactation and until 30 weeks of age) accelerates insulitis development in a mouse model of type 1 diabetes^[3].
Perfluoroundecanoic acid (0.1-1.0 mg/kg, p.o., daily, 28-35 days) induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice^[4].

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

Animal Model:	5-week-old female BALB/c nude mice were intraperitoneally coinjected pretreated RAW264.7 cells and SKOV3 cells, with observation for 4 weeks^[1]
Dosage:	8 μM pretreated RAW264.7 cells
Administration:	Co-injected intraperitoneally with SKOV3 cells for 4 weeks
Result:	Increased the number and weight of ovarian cancer metastatic nodules. Reduced the number and weight of ovarian cancer metastatic nodules in the above mouse model when pretreated with β-catenin inhibitor ICG001.

Animal Model:	35 days old Sprague-Dawley rats^[2]
Dosage:	1, 5, 10 mg/kg
Administration:	p.o. daily for 21-35 days
Result:	Reduced serum testosterone at ≥1 mg/kg; no effect on serum estradiol. Reduced serum LH at ≥1 mg/kg and serum FSH at 5 and 10 mg/kg. Down-regulated expression of Lhb and Fshb in the pituitary at 5 and/or 10 mg/kg; up-regulated Gnrhr expression at 10 mg/kg. Reduced Leydig cell number (CYP11A1-positive and HSD11B1-positive) at 5 and 10 mg/kg; no effect on Sertoli cell number. Down-regulated expression of steroidogenesis-related genes (Lhcgr, Scarb1, Star, Cyp11a1) and their proteins in the testis at various doses. Reduced sperm in the epididymis caput, corpus, and cauda at 10 mg/kg. Increased testicular triglyceride levels at 5 and 10 mg/kg; no effect on testicular total cholesterol. Down-regulated expression of Sod1 and Sod2 in the testis at various doses; increased MDA levels at 10 mg/kg. Increased LC3B and p62 levels. Reduced Beclin1 at 5 and 10 mg/kg. Reduced phosphorylation of mTOR, AKT1, AKT2, and ERK1/2. Reduced BCL2 levels at 5 and 10 mg/kg; increased BAX level at 10 mg/kg.

Animal Model:	Female non-obese diabetic (NOD) mice (offspring of 8-week-old females and 10-week-old males)^[3]
Dosage:	3, 30, 300 μg/L in drinking water
Administration:	p.o. from mating through gestation, lactation and until 30 weeks of age
Result:	Increased pancreatic insulitis grade at 11 weeks of age (300 μg/L). Increased number of apoptotic cells in pancreatic islets with insulitis grade 0 at 11 weeks of age (300 μg/L). Reduced peritoneal macrophage phagocytosis at 7 weeks of age (300 μg/L). Increased ConA-induced IL-2 secretion and decreased LPS-induced IL-6 secretion in splenocytes at 11 weeks of age (3 μg/L). Showed a trend of increased ConA-induced IL-6 and IFN-γ secretion in splenocytes at 11 weeks of age (300 μg/L). Had no significant effect on accelerating diabetes development, and low doses (3, 30 μg/L) tended to reduce diabetes incidence.

Animal Model:	Male Swiss mice (8 or 13 weeks old)^[4]
Dosage:	0.1, 0.3, 0.5, 0.7, 1.0 mg/kg
Administration:	p.o. for 28-35 days
Result:	Induced significant hepatic DNA damage. Caused reproductive toxicity: reduced sperm count and motility, increased sperm abnormalities; elevated serum LH and FSH, reduced testosterone; testicular atrophy and histopathological lesions. Altered hematological parameters: decreased PCV, Hb, platelets, RBC count and indices; increased WBC and neutrophils. Disrupted clinical biochemistry: elevated AST, ALT, urea, total cholesterol, triglyceride; reduced ALP, albumin, creatinine, HDL. Induced oxidative stress in liver and testis: increased SOD, CAT, GST, MDA; reduced GPx, GSH. Caused histopathological lesions in liver (cellular infiltration, venous congestion) and kidney (interstitial congestion, tubular lumen expansion); no spleen lesions.

Molecular Weight

564.09

Formula

C₁₁HF₂₁O₂

CAS No.

2058-94-8

Appearance

Solid

Color

White to off-white

SMILES

O=C(C(F)(C(F)(C(F)(C(F)(C(F)(C(F)(C(F)(C(F)(C(F)(C(F)(F)F)F)F)F)F)F)F)F)F)F)O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Solvent & Solubility

In Vitro:

DMSO : 200 mg/mL (354.55 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions

Concentration Solvent Mass	1 mg	5 mg	10 mg

1 mM	1.7728 mL	8.8638 mL	17.7277 mL
5 mM	0.3546 mL	1.7728 mL	3.5455 mL
10 mM	0.1773 mL	0.8864 mL	1.7728 mL

View the Complete Stock Solution Preparation Table

* 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. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

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

Concentration _(start) × Volume _(start) = Concentration _(final) × Volume _(final)

This equation is commonly abbreviated as: C₁V₁ = C₂V₂

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In Vivo Dissolution Calculator

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

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Working solution concentration: mg/mL

Purity & Documentation

Purity: 99.85%

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Data Sheet (283 KB) SDS (557 KB)

COA (247 KB) HNMR (114 KB) CNMR (130 KB) GC (214 KB)

Handling Instructions (2659 KB)

References

[1]. Cui Z, et al. PFDA promotes cancer metastasis through macrophage M2 polarization mediated by Wnt/β-catenin signaling. Chemosphere. 2024 Aug;362:142758. [Content Brief]

[2]. Yan H, et al. Perfluoroundecanoic acid inhibits Leydig cell development in pubertal male rats via inducing oxidative stress and autophagy. Toxicol Appl Pharmacol. 2021 Mar 15;415:115440. [Content Brief]

[3]. Bodin J, et al. Exposure to perfluoroundecanoic acid (PFUnDA) accelerates insulitis development in a mouse model of type 1 diabetes. Toxicol Rep. 2016 Aug 29;3:664-672. [Content Brief]

[4]. Ogunsuyi OM, et al. Perfluoroundecanoic acid induces DNA damage, reproductive and pathophysiological dysfunctions via oxidative stress in male Swiss mice. Chemosphere. 2023 Oct;338:139491. [Content Brief]

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg

DMSO	1 mM	1.7728 mL	8.8638 mL	17.7277 mL	44.3192 mL
	5 mM	0.3546 mL	1.7728 mL	3.5455 mL	8.8638 mL
	10 mM	0.1773 mL	0.8864 mL	1.7728 mL	4.4319 mL
	15 mM	0.1182 mL	0.5909 mL	1.1818 mL	2.9546 mL
	20 mM	0.0886 mL	0.4432 mL	0.8864 mL	2.2160 mL
	25 mM	0.0709 mL	0.3546 mL	0.7091 mL	1.7728 mL
	30 mM	0.0591 mL	0.2955 mL	0.5909 mL	1.4773 mL
	40 mM	0.0443 mL	0.2216 mL	0.4432 mL	1.1080 mL
	50 mM	0.0355 mL	0.1773 mL	0.3546 mL	0.8864 mL
	60 mM	0.0295 mL	0.1477 mL	0.2955 mL	0.7387 mL
	80 mM	0.0222 mL	0.1108 mL	0.2216 mL	0.5540 mL
	100 mM	0.0177 mL	0.0886 mL	0.1773 mL	0.4432 mL