Poly-L-lysine (hydrobromide) (MW 30000-70000)

Name: Poly-L-lysine (hydrobromide) (MW 30000-70000)
Brand: MedChemExpress
SKU: HY-126437
Rating: 4.5 (1 reviews)

Cat. No.: HY-126437: FAQs
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Poly-L-lysine hydrobromide (MW 30000-70000) is a water-soluble synthetic polypeptide. Poly-L-lysine hydrobromide (MW 30000-70000) downregulates Bcl-2 and upregulates Bax and p53 proteins. Poly-L-lysine hydrobromide (MW 30000-70000) promotes Apoptosis and reduces VEGF expression. Poly-L-lysine hydrobromide (MW 30000-70000) shows anticancer activity against a variety of tumors. Poly-L-lysine hydrobromide (MW 30000-70000) can also be used as a coating material.

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

Poly-L-lysine (hydrobromide) (MW 30000-70000) Chemical Structure

CAS No. : 25988-63-0

Size	Stock	Quantity
5 mg	In-stock	Estimated Time of Arrival: December 31
10 mg	In-stock	Estimated Time of Arrival: December 31
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Based on 1 publication(s) in Google Scholar

Other Forms of Poly-L-lysine (hydrobromide) (MW 30000-70000):

Poly-L-lysine hydrochloride Get quote
Poly-L-lysine hydrobromide (MW 70000-150000) Get quote
Poly-L-lysine (hydrobromide) (MW 150000-300000) Get quote
Poly-L-lysine hydrobromide (MW ＞300000) Get quote
Poly-L-lysine hydrobromide (MW 15000-30000) Get quote
Poly-L-lysine hydrobromide (MW 4000-15000) Get quote
Poly-L-lysine hydrobromide (MW 1000-5000) Get quote
Poly-L-lysine solution (0.01%, sterile-filtered, MW 150000-300000) Get quote

1 Publications Citing Use of MCE Poly-L-lysine (hydrobromide) (MW 30000-70000)

•Sci Adv. 2023 Jun 2;9(22):eadg3365. [Abstract]

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VEGFR1/Flt-1 VEGFR2/KDR/Flk-1 VEGFR3/Flt-4

Biological Activity
Purity & Documentation
References
Customer Review

Description

IC₅₀ & Target^[1]^[2]^[3]^[4]^[5]^[6]^[7]^[8]

Bax

Bcl-2

In Vitro

Poly-L-lysine hydrobromide (MW 30000-70000) ( 0.1-25 µg/mL, 24 h) shows anti-proliferative activities against human cancer cells, with IC₅₀ values of 3.36 µM, 8.23 µM, 3.53 µM and 6.04 µM for K562, A549, U937, and B16F10 cells respectively^[2].
Poly-L-lysine hydrobromide (MW 30000-70000) (0.5-40 µg/mL, 48 h) shows antiproliferative activity in MCF-7 cells (an IC₅₀ value of 4.22 µg/mL)^[3].
Poly-L-lysine hydrobromide (MW 30000-70000) (0.5-30.0 μg/mL, 24-72 h) decreases cell proliferation in in-vitro HUVECs and DAL cells, with alteration in cellular morphology in DAL cells^[4].
Poly-L-lysine hydrobromide (MW 30000-70000) (0-200 μg/mL) stimulates arachidonic acid release in cultures of 3T3 Swiss mouse fibroblasts biosynthetically labeled with [³H]arachidonic acid^[5].
Poly-L-lysine hydrobromide (MW 30000-70000) (at the working pH, isoelectric point ∼10.5)/heparin multilayer coatings prevent blood protein adsorption^[6].
Poly-L-lysine hydrobromide (MW 30000-70000) (1.0-40.0 μg/mL, 48 h) inhibits the proliferation of MDA-MB-231 and B16F10 cancer cells^[7].
Poly-L-lysine hydrobromide (MW 30000-70000) (10-120 μg/mL, 2-4 h) dose-dependently decreases viability of HeLa cells^[8].

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

Cell Viability Assay^[2]

Cell Line:	K562, A549, U937, and B16F10 cells
Concentration:	0.1, 0.5,1, 5, 10, 20, 25 µg/mL
Incubation Time:	24 h
Result:	Showed anti-proliferative activities in cancers cells (K562, A549, U937, and B16F10). Was the most potent in K562 cells.

In Vivo

Poly-L-lysine hydrobromide (MW 30000-70000) (20-40mg/kg, i.p., 14 days) inhibits Ehrlich Ascites Carcinoma (EAC), with apoptosis of EAC cells in mice^[2].
Poly-L-lysine hydrobromide (MW 30000-70000) (20-40mg/kg, i.p., 21 days) inhibits sarcoma-180 solid tumor in Swiss female albino mice^[2].
Poly-L-lysine hydrobromide (MW 30000-70000) (20-40mg/kg, i.p., starts 10 days after tumor inoculations and was continued for 21 days) inhibits DAL solid tumor growth in mice^[4].
Poly-L-lysine hydrobromide (MW 30000-70000) (20-40mg/kg, i.p., starts 10 days after tumor inoculations and was continued for 21 days) induces apoptosis in 2D and 3D tumor microenvironment of both MDA-MB-231 and B16F10 induced mice model^[7].

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

Animal Model:	EAC tumor bearing mouse (inoculated with 0.1 ml of tumor cell suspension, prepared in phosphate buffer solution containing 2×10⁶ cells/mL)^[2]
Dosage:	20, 40 mg/kg
Administration:	Intraperitoneal injection (i.p.), 14 days
Result:	Reduced the ascite fluid volume, packed cell volume and viable tumor cell count, whereas, increased non-viable tumor cell count in a dose dependent manner. Increased the hemoglobin counts towards the normal levels. Showed chromatin condensation, blebbing of plasma membrane, irregularity in cell morphology (EAC). Inhibited peritoneal angiogenesis. Showed apoptosis of EAC cells.

Animal Model:	Sarcoma-180 solid tumor model (given subcutaneous inoculation (s.c.) of 0.1 ml sarcoma-180 cell suspension containing 2×10⁶ cells/mL)^[2]
Dosage:	20, 40 mg/kg
Administration:	Intraperitoneal injection (i.p.), 21 days
Result:	Inhibited tumor growth. Could bring down the WBC level compare to Sarcoma-180 control group. Enhanced the survival of sarcoma-180 bearing mice. Showed less proliferation and muscle invasion in extents areas of coagulative necrosis. Induced cell apoptosis by triggering the expression of p53 and Bcl-2.

Molecular Weight

30000-70000

Formula

C₈H₁₉BrN₂O

CAS No.

25988-63-0

Appearance

Solid

Color

White to off-white

SMILES

CN[C@@H](CCCC[NH3+])C(C)=O.[n].[Br-].[n]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

-20°C, protect from light, stored under nitrogen

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

Solvent & Solubility

In Vitro:

H₂O : 100 mg/mL (Need ultrasonic)

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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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This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.

The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).

Purity & Documentation

Select Batch:

Data Sheet (279 KB) SDS (393 KB)

COA (246 KB)

Handling Instructions (2659 KB)

References

[1]. Archishman Ghosh, et al. Three archetypical classes of macromolecular regulators of protein liquid-liquid phase separation. Proc Natl Acad Sci U S A. 2019;116(39):19474-19483. [Content Brief]

[2]. Debnath S, et al. Poly-L-Lysine Inhibits Tumor Angiogenesis and Induces Apoptosis in Ehrlich Ascites Carcinoma and in Sarcoma S-180 Tumor. Asian Pac J Cancer Prev. 2017 Aug 27;18(8):2255-2268. [Content Brief]

[3]. Mukherjee A, et al. DNA interactive property of poly-L-lysine induces apoptosis in MCF-7 cells through DNA interaction. J Biochem Mol Toxicol. 2023 Aug;37(8):e23378. [Content Brief]

[4]. Debnath S, et al. Induction of apoptosis, anti-proliferation, tumor-angiogenic suppression and down-regulation of Dalton's Ascitic Lymphoma (DAL) induced tumorigenesis by poly-l-lysine: A mechanistic study. Biomed Pharmacother. 2018 Jun;102:1064-1076. [Content Brief]

[5]. Shier WT, et al. Polycations as prostaglandin synthesis inducers. Stimulation of arachidonic acid release and prostaglandin synthesis in cultured fibroblasts by poly(L-lysine) and other synthetic polycations. Biochim Biophys Acta. 1984 Apr 18;793(2):238-50. [Content Brief]

[6]. Barrantes A, et al. Poly-l-lysine/heparin multilayer coatings prevent blood protein adsorption. J Colloid Interface Sci. 2017 Jan 1;485:288-295. [Content Brief]

[7]. Debnath S, et al. Poly-l-Lysine inhibits VEGF and c-Myc mediated tumor-angiogenesis and induces apoptosis in 2D and 3D tumor microenvironment of both MDA-MB-231 and B16F10 induced mice model. Int J Biol Macromol. 2021 Jul 31;183:528-548. [Content Brief]

[8]. Lin CW, et al. Protective role of autophagy in branched polyethylenimine (25K)- and poly(L-lysine) (30-70K)-induced cell death. Eur J Pharm Sci. 2012 Dec 18;47(5):865-74. [Content Brief]