ABT-639 / AbbVie - LARVOL DELTA

Effect of ABT-639 on Cav3.2 channel activity and its analgesic actions in mouse models of inflammatory and neuropathic pain. (PubMed, Eur J Pharmacol) - "In the CFA model, both compounds reversed thermal hyperalgesia upon systemic delivery, but only Z944 mediated pain relief upon intrathecal delivery, indicating that ABT-639 acts primarily at peripheral sites. ABT-639 lost its analgesic effects in CFA treated Cav3.2 null mice, indicating that these channels are essential for ABT-639-mediated pain relief despite its poor inhibition of Cav3.2 currents."

Journal • Preclinical • Immunology • Neuralgia • Pain • CAV3

Inactivation of CACNA1H induces cell apoptosis by initiating endoplasmic reticulum stress in glioma. (PubMed, Transl Neurosci) - "T-type Ca channel inhibitors ABT-639 and NNC55-0396 also induced apoptosis through ERS in glioma cells. Our data highlighted the effect of CACNA1H as an oncogenic gene in human glioma."

Journal • Brain Cancer • CNS Tumor • Glioma • Oncology • Solid Tumor • ATF6 • CACNA1H • HSPA5

The T type calcium channel CaV3.2 regulates bladder afferent responses to mechanical stimuli. (PubMed, Pain) - "In an ex vivo bladder-nerve recording preparation pharmacological inhibition of CaV3.2 with TTA-A2 and ABT-639, selective blockers of T-type calcium channels, dose-dependently attenuated bladder afferent responses to distension in the absence of changes to muscle compliance...Nocifensive visceromotor responses to noxious bladder distension in-vivo were also significantly reduced by inhibition of CaV3 with TTA-A2. Together these data provide evidence of a major role for CaV3.2 in regulating bladder afferent responses to bladder distension and nociceptive signalling to the spinal cord."

Journal • Immunology • Interstitial Cystitis • Musculoskeletal Pain • Overactive Bladder • Pain

Role of T CD4+ cells, macrophages, C-LTMRs and spinal-located Ca 3.2 calcium channels in inflammation and related pain-like symptoms in murine inflammatory models. (PubMed, Br J Pharmacol) - "This work highlights the crucial role of Ca 3.2 channels in inflammation and related pain and suggests that targeting Ca 3.2 channels with pharmacological agents could be an attractive and readily evaluable strategy in a clinical trial to relieve chronic inflammatory pain in affected patients."

Journal • Preclinical • Immunology • Inflammation • Pain • CD4

Modification of mesenchymal stem cells by HMGB1 promotes the activity of Cav3.2 T-type calcium channel via PKA/β-catenin/γ-cystathionase pathway. (PubMed, Stem Cell Res Ther) - "Our study revealed that modification of MSCs with HMGB1 promoted CACNA1H-mediated calcium influx via PKA/β-catenin/γ-cystathionase pathway. This was a plausible mechanism for high mobility of MSC-H cell line."

Journal • Cardiovascular • HMGB1

Inhibition of CACNA1H can alleviate endoplasmic reticulum stress and reduce myocardial cell apoptosis caused by myocardial infarction. (PubMed, Eur Rev Med Pharmacol Sci) - "The CACNA1H inhibitor ABT-639 can alleviate myocardial cell apoptosis caused by MI by reducing the ER stress response."

Journal • Cardiovascular • Coronary Artery Disease • Heart Failure • Myocardial Infarction • Myocardial Ischemia • CASP3 • CASP9 • PCR

Cav3.2 calcium channel inhibition: a new target for colonic hypersensitivity associated with low-grade inflammation. (PubMed, Br J Pharmacol) - "These results suggest that ethosuximide represents a promising drug reposition strategy and that Cav3.2 inhibition is an attractive therapeutic approach for relieving CHS in IBS or IBD."

Journal • CNS Disorders • Gastroenterology • Immunology • Inflammation • Inflammatory Bowel Disease • Pain

Inhibition of CACNA1H attenuates doxorubicin-induced acute cardiotoxicity by affecting endoplasmic reticulum stress. (PubMed, Biomed Pharmacother) - "CACNA1H inhibitors significantly alleviated DOX-induced cardiotoxicity and apoptosis induced by ER stress."

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