1. GPCR/G Protein
    Neuronal Signaling
  2. Neurokinin Receptor
  3. Vapreotide acetate

Vapreotide acetate (Synonyms: RC-160 acetate; BMY-41606 acetate)

Cat. No.: HY-P0061A Purity: 99.77%
Handling Instructions

Vapreotide acetate (RC-160 acetate; BMY-41606 acetate) is a neurokinin-1 (NK1) receptor antagonist, with an IC50 of 330 nM.

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

Vapreotide acetate Chemical Structure

Vapreotide acetate Chemical Structure

CAS No. : 849479-74-9

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Based on 1 publication(s) in Google Scholar

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Vapreotide acetate (RC-160 acetate; BMY-41606 acetate) is a neurokinin-1 (NK1) receptor antagonist, with an IC50 of 330 nM.

In Vitro

Vapreotide attenuates the Substance P (SP)-triggered intracellular calcium increases and NF-κB activation in a dose-dependent manner. Vapreotide also inhibits SP-induced IL-8 and MCP-1 production in HEK293-NK1R and U373MG cell lines. Vapreotide inhibits HIV-1 infection of human MDM in vitro, an effect that is reversible by SP pretreatment[1]. Vapreotide significantly inhibits GH-, PRL, and/or alpha-subunit release by human GH-secreting pituitary adenoma cells in concentrations as low as 10-12-10-14 M. Vapreotide inhibits GH release with an IC50 of 0.1 pM[2]. Vapreotide exhibits moderate-to-high affinities for SSTR2, -3, and -5 (IC50=0.17, 0.1 and 21 nM, respectively) and low affinity for SSTR1 and -4 (IC50=200 and 620 nM, respectively). RC-160 inhibits serum-induced proliferation of CHO cells expressing SSTR2 and SSTR5 (EC50=53 and 150 pM, respectively)[3].

In Vivo

In cirrhosis, bleeding by rupture of oesophagogastric varices is a severe complication of portal hypertension. The acute administration of vapreotide to rats decreases collateral circulation blood flow while chronic administration attenuated its development[4]. Tumor volumes and weights are reduced by about 40% by RC-160 by s.c. injections at doses of 100 μg/day/animal. Vapreotide can inhibit the growth of androgen-independent prostate cancer when the therapy is started at an early stage of tumor development[5].

Clinical Trial
Molecular Weight







OC(C)=O.[FCYWKVCW-NH2(Disulfide bridge: Cys2-Cys7)]


Room temperature in continental US; may vary elsewhere.

Powder -80°C 2 years
-20°C 1 year
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

H2O : 14.29 mg/mL (11.99 mM; Need ultrasonic)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 0.8394 mL 4.1968 mL 8.3936 mL
5 mM 0.1679 mL 0.8394 mL 1.6787 mL
10 mM 0.0839 mL 0.4197 mL 0.8394 mL
*Please refer to the solubility information to select the appropriate solvent.
Cell Assay

CHO cells are cultured in aMEM containing 10% FCS. After overnight attachment, the medium is changed to a MEM containing either 10% FCS or insulin with and without vapreotide. Cell growth is measured after 24 h by counting cells with a Coulter counter model ZM[3].

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

Animal Administration

Rats: Acute effects are evaluated at baseline and 30 min after placebo or vapreotide (8 μg/kg/hr) infusions in DMNA rats. Chronic hemodynamic effects are evaluated using subcutaneous implants for five weeks in anesthetized DMNA rats and in sham rats. Hemodynamic measurements include splenorenal shunt blood flow by the transit time ultrasound method and cardiac output by the combined dilution–TTU method[4].

Mice: Nude mice bearing xenografts of the androgen-independent human prostate-cancer cell line PC-3 are treated for 4 weeks with somatostatin analog vapreotide (20 μg/day/animal), bombesin/gastrin-releasing peptide (GRP) antagonist, or the combination of both peptides. Tumor volumes and weights are measured[5].

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


Purity: 99.77%

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VapreotideRC-160BMY-41606RC160RC 160BMY41606BMY 41606Neurokinin ReceptorNK receptorInhibitorinhibitorinhibit

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