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Last update 08 May 2025

ABCC9

Last update 08 May 2025

Basic Info

Synonyms

ABCC9, ATP binding cassette subfamily C member 9, ATP-binding cassette sub-family C member 9

+ [4]

Introduction

Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with KCNJ11. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation (PubMed:9831708). Can form a sulfonylurea-sensitive but ATP-insensitive potassium channel with KCNJ8 (By similarity).

Drugs associated with ABCC9

Minoxidil

Target

ABCC9 x Kir6.2

Mechanism

ABCC9 agonists [+1]

Active Org.

JOHNSON AND JOHNSON GROUP CONSUMER COMPANIES [+4]

Originator Org.

Pfizer Inc.

Active Indication

Hypertension [+5]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

United States

First Approval Date18 Oct 1979

VU-0542270

Target

ABCC9 x KCNJ8

Mechanism

ABCC9 inhibitors [+1]

Active Org.

Vanderbilt University

Originator Org.

Vanderbilt University

Active Indication

Cardiovascular Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

173

Clinical Trials associated with ABCC9

CTRI/2025/04/085182

/ Not yet recruitingPhase 3IIT

Comparing the efficacy and safety of 5% topical minoxidil combined with oral bicalutamide versus 5% topical minoxidil in the treatment of female pattern hair loss: A randomized controlled trial

Start Date06 Apr 2026

Sponsor / Collaborator-

NCT06924632

/ Not yet recruitingPhase 3

Phase 3, Multicentre, Randomised, Double-Blinded, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Minoxidil Sublingual (SL) Tablet (2.5 mg) Twice Daily (BID) in the Treatment of Male Androgenetic Alopecia (AGA) in Adults

This is a phase 3, multicentre, randomised, double-blinded, placebo-controlled study examining the safety and efficacy of 2.5 mg sublingual (SL) minoxidil tablets taken twice daily in the treatment of androgenetic alopecia (AGA) in men. The duration of study participation is 32 weeks including screening and safety follow up.
The primary efficacy objective is to determine whether treatment with 2.5 mg SL tablets twice daily increases the number of hairs in men with AGA over 24 weeks. The primary safety objective is to evaluate the safety and tolerability of 2.5 mg SL tablets administered twice daily over 24 weeks.

Start Date01 Jul 2025

Sponsor / Collaborator-

CTRI/2025/03/082882

/ Not yet recruitingNot ApplicableIIT

Randomised prospective case control study on Low dose oral minoxidil 1.25mg in maleandrogenetic alopecia (AGA), and to compare the pre- and post-treatment dermoscopicfeatures in male androgenetic alopecia (AGA).

Start Date01 Apr 2025

Sponsor / Collaborator-

100 Clinical Results associated with ABCC9

100 Translational Medicine associated with ABCC9

0 Patents (Medical) associated with ABCC9

212

Literatures (Medical) associated with ABCC9

01 Jul 2025·Journal of Hazardous Materials

The tolerance mechanism of diarrhetic shellfish toxins mediated by the extracellular regulated protein kinase (ERK) pathway in the mussel Perna viridis

Article

Author: Li, Hong-Ye ; Lv, Jin-Jin ; Deng, Li-Yan ; Liu, Yu-Jie ; Mo, Yan-Hang ; Liu, Yang ; Zhang, Li ; Yang, Wei-Dong

Diarrheic shellfish toxins (DSTs) are a class of lipophilic algal toxins that accumulate excessively in bivalves following harmful algal blooms. Bivalves exhibit tolerance to DSTs, which make people ignore or underestimate the risk of DSTs, leading to the occurrence of seafood poisoning incidents. However, the tolerance mechanism remains unclear in bivalves. We investigated the role of extracellular-regulated protein kinase (ERK) in DSTs tolerance, and observed that the ERK inhibitor PD98059 exacerbated damage of DSTs to the digestive tubules. PD98059 induced the TUNEL fluorescence intensity, and caspase-3 activity inhibited by DSTs were restored to the control. PD98059 enhanced the fluorescence intensity of extracellular Ca-AM and increased the accumulation of esterified DSTs. Transcriptome analysis revealed that PD98059 affected the genes expression related to apoptosis, ABC transporters, and lipid metabolism. qPCR analysis demonstrated that PD98059 down-regulated the DSTs-induced iap and ABCC10 (p = 0.063), and up-regulated ABCB1-like1, ABCC1, ABCC1-like1, and ABCC9. Molecular docking suggested that ABCC10 exhibited high affinity for esterified okadaic acid. Overall, ERK plays a crucial role in DSTs tolerance by regulating the anti-apoptotic system and ABC transporters in bivalves. Our study is of great significance to understand the tolerance mechanism in bivalves and the safety risk caused by DSTs.

01 May 2025·Brain Pathology

Nicorandil treatment improves survival and spatial learning in aged granulin knockout mice

Article

Author: Niedowicz, Dana M. ; Nelson, Peter T. ; Norris, Christopher M. ; Fister, Shuling ; Prajapati, Paresh ; Sompol, Pradoldej ; Zhong, Yu ; Patel, Indumati ; Rogers, Colin B. ; Saatman, Kathryn E. ; Powell, David K. ; Wang, Wang‐Xia

AbstractMutations in the human granulin (GRN) gene are associated with multiple diseases, including dementia disorders such as frontotemporal dementia (FTD) and limbic‐predominant age‐related TDP‐43 encephalopathy (LATE). We studied a Grn knockout (Grn‐KO) mouse model in order to evaluate a potential therapeutic strategy for these diseases using nicorandil, a commercially available agonist for the ABCC9/Abcc9‐encoded regulatory subunit of the “K+ATP” channel that is well‐tolerated in humans. Aged (13 months) Grn‐KO and wild‐type (WT) mice were treated as controls or with nicorandil (15 mg/kg/day) in drinking water for 7 months, then tested for neurobehavioral performance, neuropathology, and gene expression. Mortality was significantly higher for aged Grn‐KO mice (particularly females), but there was a conspicuous improvement in survival for both sexes treated with nicorandil. Grn‐KO mice performed worse on some cognitive tests than WT mice, but Morris Water Maze performance was improved with nicorandil treatment. Neuropathologically, Grn‐KO mice had significantly increased levels of glial fibrillary acidic protein (GFAP)‐immunoreactive astrocytosis but not ionized calcium binding adaptor molecule 1 (IBA‐1)‐immunoreactive microgliosis, indicating cell‐specific inflammation in the brain. Expression of several astrocyte‐enriched genes, including Gfap, were also elevated in the Grn‐KO brain. Nicorandil treatment was associated with a subtle shift in a subset of detected brain transcript levels, mostly related to attenuated inflammatory markers. Nicorandil treatment improved survival outcomes, cognition, and inflammation in aged Grn‐KO mice.

27 Mar 2025·JCEM Case Reports

Cantú Syndrome With Acromegaloid Features, Multiple Endocrinopathies, and Infection Susceptibility

Article

Author: Jönsson, Göran ; Karlsson, Ulf ; Nygren, David ; Moll, Ulrika ; Braun, Oscar

AbstractCantú syndrome involves fetal polyhydramniosis, congenital hypertrichosis, and macrosomia. Distinctive features include acromegaloid features with broad nasal bridge and macroglossia as well as cardiac abnormalities, including patent ductus arteriosus. We present a case in a male patient, who presented with cardiac abnormalities in childhood, but was diagnosed with the syndrome in adulthood after many years of atypical symptoms such as multiple endocrinopathies and infection susceptibility. He had surgery for a patent ductus arteriosus in early childhood. During adulthood, he developed idiopathic pericarditis. Extensive rheumatological investigations were made, and in parallel, several endocrinopathies were found. These included thyroiditis with subsequent hypothyroidism, idiopathic partial hypocortisolism, and GH insufficiency. In addition, he had mild neutropenia and required hospitalization twice because of Streptococcus pyogenes infections. Immunodeficiency screening has not revealed a specific primary immunodeficiency, yet transient neutropenia, low count of CD8+ effector memory T cells, as well as lymphocyte responses, was seen during bacteremia. The diagnose was made after a trio-whole genome sequencing identified a pathogenic missense variant of the gene ABCC9 (c.3460C > T;p. (Arg1154Trp)) causing Cantú syndrome.

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ABCC9

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