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Last update 20 Mar 2025

Chloropyramine Hydrochloride

Last update 20 Mar 2025

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

C9, Chloropyramine, Chlorpyramine

+ [13]

Target

H1 receptor

Action

antagonists

Mechanism

H1 receptor antagonists(Histamine H1 receptor antagonists)

Therapeutic Areas

Immune System DiseasesInfectious DiseasesEye Diseases+ [2]

Active Indication

AsthmaConjunctivitis, AllergicRhinitis, Allergic

Inactive Indication-

Originator Organization-

Active Organization-

Inactive Organization-

Drug Highest PhaseApproved

First Approval Date-

Regulation-

Structure/Sequence

Molecular FormulaC16H20ClN3

InChIKeyICKFFNBDFNZJSX-UHFFFAOYSA-N

CAS Registry59-32-5

View All Structures (2)

100 Clinical Results associated with Chloropyramine Hydrochloride

100 Translational Medicine associated with Chloropyramine Hydrochloride

100 Patents (Medical) associated with Chloropyramine Hydrochloride

478

Literatures (Medical) associated with Chloropyramine Hydrochloride

16 Feb 2025·Future Medicinal Chemistry

Pioneering first-in-class HDAC-ROCK inhibitors as potential multitarget anticancer agents

Article

Author: Beljkas, Milan ; Oljacic, Slavica ; Djuric, Ana ; Ruzic, Dusan ; Jallet, Corinne ; Nikolic, Katarina ; Vuletic, Ana ; Petkovic, Milos ; Cadet-Daniel, Véronique ; Santibanez, Juan F. ; Arimondo, Paola B. ; Srdic-Rajic, Tatjana ; Tchiehe, Guilaine Nchugoua

AIMWith the aim of simultaneously modulating the epigenetic system and the protein kinase pathway, we selected the enzyme histone deacetylase (HDAC) and the Rho-associated protein kinases (ROCK) as desired targets to develop potential multitarget anticancer agents with additional antimetastatic properties. We report here the rational design, synthesis, and biological evaluation of the first-in-class HDAC/ROCK multitarget inhibitors in pancreatic ductal adenocarcinoma (PDAC) and triple-negative breast cancer (TNBC).MATERIALS AND METHODSA molecular docking study performed with the Gold software was used to develop HDAC/ROCK multitarget inhibitors. IC₅₀ values were determined by enzyme assays. The cytotoxicity, anti-migratory and anti-invasive properties of the inhibitors were evaluated using triple-negative breast cancer cells (MDA-MB-231 and HCC 1973) and pancreatic ductal adenocarcinoma cells (Panc-1 and MiaPaCa-2).RESULTSC-9 showed significant inhibition of HDAC6, ROCK1 and ROCK2. At the same time, this compound showed strong antiproliferative effects on MDA-MB-231, MiaPaCa-2 and Panc-1 cell lines with IC₅₀ values of 5.81 μM, 3.87 μM and 19.57 μM. In addition, it demonstrated great anti-invasive and anti-migratory effects.CONCLUSIONThe findings of this study strongly suggest that the simultaneous inhibition of ROCK and HDACs holds significant potential as a promising therapeutic strategy in the advancement of cancer treatment.

01 Feb 2025·Future Medicinal Chemistry

Dual delivery of metformin and Y15 from a PLGA scaffold for the treatment of platinum-resistant ovarian cancer

Article

Author: Garcia, Kristal ; Jordan, Emily ; Arriaga, Marco A. ; Obregon, Hannah ; Chew, Sue Anne ; Villalobos, Viviana ; Levy, Arkene ; Duarte, Manuel A.

AIMSDrug-loaded poly(lactic-co-glycolic acid) (PLGA) scaffolds were fabricated using a mold-less technique to investigate whether the combined delivery of both Y15 (FAK inhibitor) and metformin would result in enhanced effects on cell viability compared to the release of each drug alone for the treatment of platinum-resistant ovarian cancer (PROC).MATERIALS & METHODSScaffolds were fabricated using an easy and economical mold-less technique that combined PLGA and the drugs (i.e. metformin and/or Y15) in tetraglycol and injected in PBS, to form a globular morphology.RESULTSThe exposure of cells to metformin and Y15 resulted in a significantly enhanced cytotoxic efficacy compared to single-drug treatment with either metformin or Y15. When the drugs were delivered using the PLGA scaffolds, the combination of the two drugs was significantly more cytotoxic compared to scaffolds containing metformin only and Y15 only.CONCLUSIONSThe combination of metformin and Y15 can result in an increase in antitumor activity in PROC cells through apoptosis. The delivery of both drugs from the PLGA biomaterial scaffold allowed for a more enhanced combinational effect compared to the utilization of free drugs (without a scaffold) and should be further explored as a promising treatment of PROC.

01 Nov 2024·International Journal of Biological Macromolecules

Effects of pleiotrophin (PTN) on the FAK inhibitor Y15 in breast cancer cells

Article

Author: Yao, Jiaxin ; Yang, Liquan ; Ding, Linlin ; You, Liwei ; Li, Yunfei ; Zhang, Yuqiang ; Liu, Huali ; Lin, Xueyuan ; Qu, Siyang

Overexpression of PTN (Pleiotrophin) in breast cancer cells stimulates breast cell proliferation and anti-apoptosis via the FAK/Src signaling pathway.1,2,4,5-Benzenetetramine tetrahydrochloride (C₆H₁₄Cl₄N₄) known as Y15 is an inhibitor that specifically blocks phosphorylation of Y397-FAK and total FAK phosphorylation. The exogenous PTN protein was induced to be expressed by a prokaryotic expression strain. The addition of PTN protein decreased the sensitivity of breast cancer cells to Y15, as shown by both MTT and flow cytometry assays. Breast cancer cells transfected with sh-RNA knockdown PTN were analyzed by real-time fluorescence quantitative PCR reaction (RT-PCR) and protein immunoblotting 24 h after transfection. MTT assay data showed a significant increase in the IC50 value of Y15 against breast cancer cells in the presence of PTN protein. Flow cytometry data confirmed the dose-dependent anti-apoptotic effect of PTN protein in Y15-treated breast cancer cells. After transfection with sh-RNA, Y15 further inhibited the FAK pathway, greatly reducing cell survival and promoting apoptosis. Western blotting analysis showed that knockdown of PTN protein with sh-RNA resulted in increased apoptosis and elevated levels of apoptotic proteins, such as cleaved PARP and cleaved caspase-3 in Y15-induced breast cancer cells. Finally, it was hypothesized that PTN and Y15 were associated with a significant increase in the IC50 value of PTN and Y15 in breast cancer cells by western blotting analysis. It was hypothesized that PTN and Y15 regulate the proliferation and apoptosis of breast cancer cells through the AKT/PI3K pathway. The results demonstrated that PTN affects the sensitivity of the kinase inhibitor Y15, and PTN silencing and Y15 may inhibit the survival of breast cancer cells through the AKT/PI3K pathway, which lays the foundation for subsequent in-depth research on the clinical treatment of breast cancer.

100 Deals associated with Chloropyramine Hydrochloride

External Link

KEGG	Wiki	ATC	Drug Bank
D07679	Chloropyramine Hydrochloride	D04AA09 R06AC03	DB08800

R&D Status

10 top approved records.

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Indication	Country/Location	Organization	Date
Asthma	-	-	-
Conjunctivitis, Allergic	-	-	-
Rhinitis, Allergic	-	-	-

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


AACR2023	Not Applicable	Platinum-Resistant Ovarian Carcinoma	-	Y15	jouryhqmcb(xjjkneqiqs) = odypjymizw regnijjuga (mykqrpcika )	-	04 Apr 2023
				Metformin	jouryhqmcb(xjjkneqiqs) = mifatfriwx regnijjuga (mykqrpcika )
AACR2022	Not Applicable	Platinum-Resistant Ovarian Carcinoma Second line	-	Y15	jlmlqyvuek(qoiufmjnbj) = nrgjwvszfp vxbssceydx (wwyuctrxzq ) View more	-	15 Jun 2022
				Metformin	jlmlqyvuek(qoiufmjnbj) = nqzivogtqo vxbssceydx (wwyuctrxzq ) View more

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Chloropyramine Hydrochloride

Overview

Basic Info

Structure/Sequence

Related

External Link

R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

Regulation