Pathways

Talbutal, also called 5-allyl-5-sec-butylbarbituric acid, is a barbiturate with a short to intermediate duration of action. It is a nonselective central nervous system (CNS) depressant. As with other barbiturates, talbutal is capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. Barbiturates may also induce anesthesia at sufficiently high therapeutic doses. Talbutal binds to GABAA receptors at a distinct binding site associated with a Cl- ionopore of the receptor. Upon binding, talbutal increases the duration of time for which the Cl- ionopore is open, leading to prolonged inhibitory effect of GABA at the postsynaptic thalamic neuron. Talbutal is a potentiator of the GABA(A) alpha-1 through alpha-6 subunits. Some side effects of using Talbutal may include drowsiness, loss or coordination, nausea, and insomnia.

Talbutal is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Talbutal passes through the liver and is then excreted from the body mainly through the kidney.

Tamoxifen is a selective estrogen modulator (SERM) used in the treatment of estrogen-sensitive breast cancer. Tamoxifen itself only has weak anti-estrogen effects and must be converted into more active metabolites to have therapeutic activity. Metabolism takes place in the liver and is carried out primarily by cytochrome P450 enzymes. Tamoxifen is hydroxylated by CYP2D6 and demethylated by CYP3A4 and CYP3A5, producing the active metabolites 4-hydroxytamoxifen and endoxifen. These metabolites inhibit estrogen binding to estrogen receptors in breast cancer cells, which in turn inhibit tumour growth.

Tamoxifen is an anticancer drug that is a selective estrogen receptor modulator also known as a non-steroidal anti-estrogen. It is used to treat estrogen receptor positive breast cancer as well for reducing the risk of invasive breast cancer post surgery. It is also prescribed as a prophylaxis for women with a high risk of breast cancer. It's often prescribed alone or possible as an adjuvant in other treatments. Tamoxifen's mechanism of action works by inhibiting the growth of tumor cells while also promoting apoptosis. It competitively inhibits estrogen/estradiol binding to its receptor which prevents the coactivator from binding to the receptor-tamoxifen complex in the nucleus. This prevents transcription of the estrogen target genes decreasing the production of tumor growth factor alpha and insulin-like growth factor 1 while increasing sex hormone binding globulin. Tamoxifen is also shown to induce apoptosis in estrogen receptor positive cancer cells. The action might be due to the inhibition of protein kinase C (PKC) which inhibits DNA synthesis. Overdose of tamoxifen leads to acute neurotoxicity seen by tremors, hyperreflexia, unsteady gait, and dizziness. Tamoxifen is usually administered in an oral form in a tablet or solution form.

Tamoxifen is a selective estrogen modulator (SERM) used in the treatment of estrogen-sensitive breast cancer. Tamoxifen itself only has weak anti-estrogen effects and must be converted into more active metabolites to have therapeutic activity. Metabolism takes place in the liver and is carried out primarily by cytochrome P450 enzymes. Tamoxifen is hydroxylated by CYP2D6 and demethylated by CYP3A4 and CYP3A5, producing the active metabolites 4-hydroxytamoxifen and endoxifen. These metabolites inhibit estrogen binding to estrogen receptors in breast cancer cells, which in turn inhibit tumour growth.

Tamsulosin is an alpha-1A and alpha-1B adrenergic receptor antagonist used to treat benign prostatic hyperplasia, ureteral stones, prostatitis, and female voiding dysfunction. Tamsulosin is a blocker of alpha-1A and alpha-1D adrenoceptors but about 70% of the alpha-1 adrenoceptors in the prostate are of the alpha-1A subtype. By blocking these adrenoceptors, smooth muscle in the prostate is relaxed and urinary flow is improved. Alpha-1A adrenergic receptor are coupled to the Gq signaling cascade. When these receptors are activated, it leads to the activation of phospholipase C, which converts Phosphatidylinositol (3,4,5)-trisphosphate to inositol (3,4,5)-trisphosphate (IP3) and diacylglycerol (DAG). IP3 activates IP3 receptors on the sarcoplasmic reticulum leading to the release of stored calcium into the cytosol. DAG activates protein kinase C (PKC). One of the downstream effects of PKC include activation of calcium channels on the membrane, leading to influx of calcium ions into the cytosol. Both IP3 and DAG increase cytosolic levels of calcium which then binds to calmodulin to create a calcium-calmodulin complex. Muscle contraction and relaxation are controlled by the enzymes myosin kinase and myosin phosphatase. Myosin kinase phosphorylates myosin light chain, leading to interaction between actin and myosin, producing muscle contraction. Myosin phosphorylase dephosphorylates the phosphorylated myosin light chain, preventing interaction with actin, producing muscle relaxation. The calcium-calmodulin activates myosin kinase, leading to increased phosphorylation of myosin light chain and more muscle contraction. By inhibiting alpha-1A receptors in the prostate, tamsulosin decreased cytosolic calcium and prevents activation of myosin kinase, thereby causing more dephosphorylation and allowing muscle relaxation. The blocking of alpha-1D adrenoceptors relaxes the detrusor muscles of the bladder which prevents storage symptoms. Alpha-1D receptors are also Gq coupled and may produce muscle relaxation in a similar mechanism to alpha-1A receptors. The specificity of tamsulosin focuses the effects to the target area while minimizing effects in other areas.