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Last update 08 May 2025

Chloropyramine Hydrochloride

Last update 08 May 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-

License 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

450

Literatures (Medical) associated with Chloropyramine Hydrochloride

01 May 2025·Biochemical and Biophysical Research Communications

FAK regulates trophoblast functions of invasion and proliferation through Rap1 pathway in early-onset preeclampsia

Article

Author: Qi, Hongbo ; Wang, Tingting ; Chen, Ruixin ; Zhang, Chen ; Jiang, Youqing ; Tong, Hai ; Zhang, Xue

This investigation examined focal adhesion kinase (FAK)'s role in trophoblast cellular processes during early-onset preeclampsia (EOPE). We analyzed FAK and its phosphorylated form (pY397FAK) expression patterns in both normal (n = 15) and EOPE (n = 15) placental tissues, including first trimester samples, using immunohistochemistry and Western blot techniques. Next, Y15 was used to inhibit FAK activity. CCK-8 detection, Western blotting, wound healing assay, Transwell assays and flow cytometry were employed to systematically evaluate FAK's impact on trophoblast cell line HTR8/SVneo. Through transcriptomic and bioinformatics analyses, we identified Rap1 as a potential downstream mediator of FAK signaling in trophoblasts. In a mouse model of preeclampsia, we found decreased expression of both FAK and Rap1 in placental tissues, supporting our in vitro findings. These results suggest that FAK may contribute to preeclampsia development by regulating trophoblast invasion and proliferation through the Rap1 signaling pathway. Our study provides insights into the molecular mechanisms underlying EOPE and identifies FAK as a potential therapeutic target for preeclampsia treatment.

01 Mar 2025·Journal of Oral Biosciences

Signaling pathways of pro-IL-1β production induced by mechanical stress in gingival epithelial cells

Article

Author: Mao, Dan ; Goda, Seiji ; Zhang, Ruixuan ; Inoue, Hiroshi ; Sougawa, Nagako

OBJECTIVESMechanical stress on the teeth and alveolar bone caused by bruxism, orthodontics, and implants affects the periodontal tissues, causing gingival recession and alveolar bone resorption, and entire body, including the heart and vascular system. Although the same forces exerted on the alveolar bone and teeth are exerted on gingival epithelial cells, little is known about the effects of mechanical stress on these cells. This study investigated the effects of mechanical stress on gingival epithelial cells.METHODSCa9-22 cells (human gingival epithelial cells) were used. They were seeded onto the silicone and stretched cyclically. Mechanical stress-stimulated Ca9-22 cells were evaluated for pro-inflammatory interleukin (pro-IL)-1β production using Western blotting and analyzed to assess the phosphorylation level of intracellular signaling molecules.RESULTSMechanical stress induced pro-IL-1β upregulation in Ca9-22 cells, which was significantly inhibited by ruthenium red. Ruthenium red significantly inhibited mechanical stress-induced phosphorylation of focal adhesion kinase (FAK), P130cas, and extracellular signal-regulated kinase 1 and 2 (ERK1/2) induced by mechanical stress. Additionally, Y15 significantly inhibited the upregulation of pro-IL-1β expression and phosphorylation of FAK, P130cas, and ERK1/2 stimulated by mechanical stress.CONCLUSIONSIn Ca9-22 cells, mechanical stress may increase pro-IL-1β production via mechanosensitive ion channels and FAK. These findings revealed the mechanisms of inflammation in mechanically-stressed Ca9-22 cells and may aid in the development of therapeutic approaches to prevent bone resorption.

16 Feb 2025·Future Medicinal Chemistry

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

Article

Author: Beljkas, Milan ; Oljacic, Slavica ; Ruzic, Dusan ; Jallet, Corinne ; Vuletic, Ana ; Nikolic, Katarina ; Djuric, 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.

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	oyretcoyou(rquocxeaoj) = yrpzxmqstg lioatyself (ukajlpawpq )	-	04 Apr 2023
				Metformin	oyretcoyou(rquocxeaoj) = mstdhxolzp lioatyself (ukajlpawpq )
AACR2022	Not Applicable	Platinum-Resistant Ovarian Carcinoma Second line	-	Y15	wschvbkoab(efjscjvfoi) = izschganjb qoblnbhmju (ndkrxuwbyd ) View more	-	15 Jun 2022
				Metformin	wschvbkoab(efjscjvfoi) = diwplnxtdu qoblnbhmju (ndkrxuwbyd ) 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