---
title: "CPD1, a water‑soluble PDE5 inhibitor, reduces pulmonary arterial hypertension via cGMP and TRPM8 m"
id: "pubmed-42035601"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42035601"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42035601/"
doi: "10.1016/j.bioorg.2026.109908"
published_at: "2026-08-05T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# CPD1, a water‑soluble PDE5 inhibitor, reduces pulmonary arterial hypertension via cGMP and TRPM8 m
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42035601
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42035601/)
- **DOI:** [10.1016/j.bioorg.2026.109908](https://doi.org/10.1016%2Fj.bioorg.2026.109908)
- **Published At:** 2026-08-05T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Pulmonary arterial hypertension (PAH) remains fatal with limited therapies; current **PDE5 inhibitors** have suboptimal aqueous solubility and incomplete mechanistic understanding. - Investigators developed a highly water‑soluble potassium salt polymorph of a PDE5 inhibitor, named **CPD1**, to address solubility and efficacy gaps. - In a monocrotaline-induced rat model of PAH, **CPD1** produced dose-dependent improvements in multiple disease measures. - CPD1 significantly reduced **pulmonary arterial pressure**, reversed **right ventricular hypertrophy**, and inhibited remodeling of small muscular pulmonary arteries in vivo. - Ex vivo vascular studies showed CPD1 attenuated enhanced contractile responses to endothelin-1, cyclopiazonic acid, and 1-oleoyl-2-acetyl-sn-glycerol in endothelium-denuded arteries. - Mechanistically, CPD1 elevates **cGMP** by inhibiting PDE5 and uniquely upregulates **TRPM8** channel expression in a dose-dependent manner. - Upregulation of TRPM8 sensitized pulmonary vasculature, markedly enhancing vasodilation from TRPM8 activation. - Authors present CPD1 as potentially first-in-class for simultaneous modulation of the **cGMP pathway** and **TRPM8**, addressing dysregulated calcium homeostasis and vascular remodeling in PAH. - The article discloses a related patent (CN201910505948.5) owned by Shenzhen Hanhui Pharmaceutical Technology Co., Ltd. - Details such as full study protocols, numerical effect sizes, safety data, and translational/clinical readiness were not reported in the PubMed abstract and require full-text consultation for confirmation.
## Clinical Analysis & Structured Key Points
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Epub 2026 Apr 22. # The novel PDE5 inhibitor CPD1 attenuates pulmonary arterial hypertension through dual modulation of cGMP and TRPM8-mediated pathways [Yunping Mu](https://pubmed.ncbi.nlm.nih.gov/?term=Mu+Y&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Jinlin Sun](https://pubmed.ncbi.nlm.nih.gov/?term=Sun+J&cauthor_id=42035601)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-2 "Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, Guangdong Province, PR China."), [Xindan Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+X&cauthor_id=42035601)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-3 "Guangzhou Quality Testing & Inspection Institute, Guangzhou, Guangdong Province, PR China."), [Huidan Zhu](https://pubmed.ncbi.nlm.nih.gov/?term=Zhu+H&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Bin Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+B&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Haoheng Qiu](https://pubmed.ncbi.nlm.nih.gov/?term=Qiu+H&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Zhenggang Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+Z&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Sujin Zhou](https://pubmed.ncbi.nlm.nih.gov/?term=Zhou+S&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Fanghong Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+F&cauthor_id=42035601)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-4 "The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: fli@gdut.edu.cn."), [Allan Zijian Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+AZ&cauthor_id=42035601)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#full-view-affiliation-5 "The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: azzhao@gdut.edu.cn.") Affiliations Expand ### Affiliations * 1 The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China. * 2 Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, Guangdong Province, PR China. * 3 Guangzhou Quality Testing & Inspection Institute, Guangzhou, Guangdong Province, PR China. * 4 The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: fli@gdut.edu.cn. * 5 The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: azzhao@gdut.edu.cn. * PMID: **42035601** * DOI: [ 10.1016/j.bioorg.2026.109908 ](https://doi.org/10.1016/j.bioorg.2026.109908) Item in Clipboard # The novel PDE5 inhibitor CPD1 attenuates pulmonary arterial hypertension through dual modulation of cGMP and TRPM8-mediated pathways Yunping Mu et al. Bioorg Chem. 2026. Show details Display options Display options Format Abstract PubMed PMID Bioorg Chem Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Bioorg+Chem%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Bioorg+Chem%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42035601/) . 2026 Aug 5:177:109908. doi: 10.1016/j.bioorg.2026.109908. Epub 2026 Apr 22. ### Authors [Yunping Mu](https://pubmed.ncbi.nlm.nih.gov/?term=Mu+Y&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Jinlin Sun](https://pubmed.ncbi.nlm.nih.gov/?term=Sun+J&cauthor_id=42035601)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-2 "Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, Guangdong Province, PR China."), [Xindan Zhang](https://pubmed.ncbi.nlm.nih.gov/?term=Zhang+X&cauthor_id=42035601)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-3 "Guangzhou Quality Testing & Inspection Institute, Guangzhou, Guangdong Province, PR China."), [Huidan Zhu](https://pubmed.ncbi.nlm.nih.gov/?term=Zhu+H&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Bin Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+B&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Haoheng Qiu](https://pubmed.ncbi.nlm.nih.gov/?term=Qiu+H&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Zhenggang Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+Z&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Sujin Zhou](https://pubmed.ncbi.nlm.nih.gov/?term=Zhou+S&cauthor_id=42035601)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-1 "The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China."), [Fanghong Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+F&cauthor_id=42035601)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-4 "The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: fli@gdut.edu.cn."), [Allan Zijian Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+AZ&cauthor_id=42035601)[ 5 ](https://pubmed.ncbi.nlm.nih.gov/42035601/#short-view-affiliation-5 "The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: azzhao@gdut.edu.cn.") ### Affiliations * 1 The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, Guangdong Province, PR China. * 2 Hui Ya Hospital of The First Affiliated Hospital, Sun Yat-Sen University, Huizhou, Guangdong Province, PR China. * 3 Guangzhou Quality Testing & Inspection Institute, Guangzhou, Guangdong Province, PR China. * 4 The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: fli@gdut.edu.cn. * 5 The International Translational Medical Research Center, Guangdong Engineering Technology Research Center of Metabolic Disorders Interdisciplinary Precision Prevention and Digital Healthcare, The Eighth Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, PR China. Electronic address: azzhao@gdut.edu.cn. * PMID: **42035601** * DOI: [ 10.1016/j.bioorg.2026.109908 ](https://doi.org/10.1016/j.bioorg.2026.109908) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Pulmonary arterial hypertension (PAH) remains a fatal condition with limited treatment options. While phosphodiesterase-5 (PDE5) inhibitors such as sildenafil and tadalafil are standard treatments, their therapeutic efficacy is limited by poor aqueous solubility and an incomplete understanding of the mechanisms underlying their long-term benefits on vascular remodeling. To overcome these critical limitations, we developed a novel, highly water-soluble potassium salt polymorph of a PDE5 inhibitor, designated CPD1. In a monocrotaline-induced rat model of PAH, CPD1 demonstrated superior in vivo efficacy. It dose-dependently alleviated key pathological hallmarks by significantly reducing pulmonary arterial pressure, reversing right ventricular hypertrophy, and inhibiting the remodeling of small muscular pulmonary arteries. At the vascular level, CPD1 significantly attenuated the enhanced contractile responses to endothelin-1, cyclopiazonic acid, and 1-oleoyl-2-acetyl-sn-glycerol in endothelium-denuded arteries. Mechanistically, we reveal a novel dual-pathway mechanism: in addition to elevating cyclic guanosine monophosphate (cGMP) through PDE5 inhibition, CPD1 uniquely and dose-dependently upregulates the expression of the transient receptor potential melastatin-8 (TRPM8) channel. This upregulation sensitizes the pulmonary vasculature, markedly enhancing vasodilation induced by TRPM8 activation. Our findings position CPD1 not merely as a more soluble PDE5 inhibitor but as a first-in-class agent that simultaneously modulates the cGMP pathway and the TRPM8 channel, offering a promising new therapeutic strategy to correct dysregulated calcium homeostasis and reverse vascular remodeling in PAH. **Keywords:** Dual-pathway mechanism; Potassium salt polymorph; Pulmonary arterial hypertension; Transient receptor potential melastatin-8; Vascular remodeling. Copyright © 2026 Elsevier Inc. All rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: The data in this article pertains to patent CN201910505948.5, which is owned by Shenzhen Hanhui Pharmaceutical Technology Co., Ltd. ## Similar articles * [ Effects of masitinib compared with tadalafil for the treatment of monocrotaline-induced pulmonary arterial hypertension in rats. ](https://pubmed.ncbi.nlm.nih.gov/31629919/) Leong ZP, Hikasa Y.Leong ZP, et al.Vascul Pharmacol. 2019 Nov-Dec;122-123:106599. doi: 10.1016/j.vph.2019.106599. Epub 2019 Oct 17.Vascul Pharmacol. 2019.PMID: 31629919 * [ C-C Motif chemokine receptor-2 blockade ameliorates pulmonary hypertension in rats and synergizes with a pulmonary vasodilator. ](https://pubmed.ncbi.nlm.nih.gov/39556088/) Tsuboya N, Sawada H, Mitani Y, Oshita H, Ohya K, Takeoka M, Kabwe JC, Miyasaka Y, Ito H, Yodoya N, Ohashi H, Maruyama J, Okamoto R, Mashimo T, Dohi K, Nishimura Y, Maruyama K, Hirayama M.Tsuboya N, et al.Cardiovasc Res. 2025 Jul 8;121(7):1076-1090. doi: 10.1093/cvr/cvae244.Cardiovasc Res. 2025.PMID: 39556088Free PMC article. * [ Tadalafil, a long-acting inhibitor of PDE5, improves pulmonary hemodynamics and survival rate of monocrotaline-induced pulmonary artery hypertension in rats. ](https://pubmed.ncbi.nlm.nih.gov/19881228/) Sawamura F, Kato M, Fujita K, Nakazawa T, Beardsworth A.Sawamura F, et al.J Pharmacol Sci. 2009 Nov;111(3):235-43. doi: 10.1254/jphs.09110fp. Epub 2009 Oct 31.J Pharmacol Sci. 2009.PMID: 19881228 * [ Phosphodiesterase 5 (PDE5): Structure-function regulation and therapeutic applications of inhibitors. ](htt
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