Fendiline or Sensit (N-(3,3-diphenylpropyl)-(1-phenylethyl)-amine), is a diphenylalkylamine blocker of L-type calcium channels. Fendiline is an anti-anginal agent for the treatment of coronary heart disease. Pharmaco-dynamically, it exerts the typical calcium as well as calmodulin antagonistic actions: inhibition of the transmembrane calcium current, smooth muscle relaxation, negative inotropism, cardioprotection, inhibition of calmodulin-activated myosin light-chain kinase and phosphodiesterase. Pharmacokinetics reveal slow onset of action and a long half-life. The anti-anginal and anti-ischaemic efficacy of fendiline has been proven in several placebo-controlled, double-blind trials. Fendiline is an FDA-approved, albeit now clinically obsolete. Additionally, fendiline is a specific inhibitor of K-Ras plasma membrane localization that also inhibits K-Ras signal output and blocks the proliferation of K-Ras-transformed tumor cells.

Dimebon (latrepirdine) is an orally available, small molecule, gamma carboline derivative that was developed and used in Russia as an over-the-counter oral antihistamine for allergy treatment since 1980s. In 1990s it was shown that Dimebon has promising potential in treating neurodegenerative diseases. In 2003, Medivation Inc acquired the rights to Dimebon. Medivation went public in December 2004, with Dimebon as the only drug in its pipeline. The product was being developed by Medivation and Pfizer as a treatment for early-stage Alzheimer's disease and Huntington's disease. However, development was discontinued by Medivation and Pfizer in early 2012. Dimebon inhibits alpha-Adrenergic receptors (alpha1A, alpha1B, alpha1D, and alpha2A), Histamine H1 and H2 receptors and Serotonin 5-HT2c, 5-HT5A, 5-HT6 receptors with high affinity. Dimebon may act by blocking NMDA receptors or voltage-gated Ca2+ channels and by preventing mitochondrial permeability pore transition.

Riodipine is the blocker of calcium channels of L-type. Riodipine is indicated for the treatment of arterial hypertension, prevention of attacks of angina pectoris. Antiepileptic effect of riodipine was manifested by a decreased frequency and amplitude of interictal discharges and a less frequent appearance of ictal discharges. Riodipine increased latency to first convulsive episodes and delayed the development of generalized tonic-clonic seizures. Detected side effects are: arterial hypotension, tachycardia, hypostasis of shins, increase of a daily urine. Allergic reactions to the drug are possible. Nitrates, tricyclic antidepressants, and other anti-hypertensive drugs are able to potentiate of riodipine effects.

Butofilolol (trade name Cafide) is a beta-blocker drug for the treatment of high blood pressure (essential hypertension). Butofilolol constitute a good therapeutic approach to hypertension in plethoric subjects when the weight reduction has failed to correct it adequately

Caroverine is a spasmolytic drug used in tinnitus treatment improves mechanosensitivity and mechanotransduction phenomenon and otoneuroprotective agent. Caroverine acts as an N-type calcium channel blocker, competitive AMPA receptor antagonist, and non-competitive NMDA receptor antagonist. When excessive glutamate binds to NMDA receptors, the receptor opens and allows calcium and sodium to enter the neuron, abnormal levels of calcium disturbs ionic balance causing spontaneous depolarization state. Pathological spontaneous depolarization state is reversed back to physiological polarization state by antagonistic property of Caroverine.

Propiverine is a well established antimuscarinic agent. It’s indicated in adults for the symptomatic treatment of urinary incontinence and/or increased urinary frequency and urgency in patients with overactive bladder syndrome or neurogenic detrusor overactivity (detrusor hyperreflexia) from spinal cord injuries, e.g. transverse legion paraplegia. As well as blocking muscarinic receptors in the detrusor muscle, the drug also inhibits cellular calcium influx, thereby diminishing muscle spasm. Overdose with the muscarinic receptor antagonist propiverine hydrochloride can potentially result in central anticholinergic effects, e.g. restlessness, dizziness, vertigo, disorders in speech and vision and muscular weakness. Moreover, severe dryness of mucosa, tachycardia and urinary retention may occur.

Brovincamine also known as brovincamine fumarate (BV, Sabromin) was used in Japan mainly as an improver of cerebral circulation and metabolism, and also as an inhibitor of the aggregation of platelets through the cyclic AMP pathway in patients with normal tension glaucoma. Brovincamine exerts its action via calcium channels blockade. The current drug status is unknown.

Budipine is an antiparkinsonian drug, which was developed by Byk Gulden (now Takeda) for the treatment of Parkinson's disease. The drug has multiple mechanisms of action: it was found to interfere with dopamine biosynthesis, mainly by inhibiting MAO-B enzyme and stimulating aromatic L-amino acid decarboxylase. Also the drug inhibits the dopamine re-uptake and has weak affinity to NMDA and muscarinic receptors. Budipine passes the blood-brain barrier, is metabolized by hydroxylation, and is excreted by both in urine and feces within 24 h.

Fomocaine is a local anesthetic used in the gel formulations for the relief of pain associated with burns and wounds. Fomocaine blocks both sodium and calcium voltage-gated ion cahnnel currents.

Zatebradine is a bradycardic compound that blocks hyperpolarization-activated inward current (If) through cyclic nucleotide-gated cation (HCN) channels in sinoatrial node cells. Additionally, it can block voltage-gated outward K+ (IK) currents and related neuronal hyperpolarization-activated inward current (Ih) channels but exhibits little or no activity for L-type Ca2+ (ICa) currents. When assessed through telemetric ECG recording in mice, zatebradine reduced heart rate from 600 to 200 beats per minute with an ED50 value of 1.8 mg/kg and induced increasing arrhythmia at concentrations >10 mg/kg.