Isoquinolines
Thalictrum
Cyclization
Actions of a pair of identified cerebral-buccal interneurons (CBI-8/9) in Aplysia that contain the peptide myomodulin. (1/2998)
A combination of biocytin back-fills of the cerebral-buccal connectives and immunocytochemistry of the cerebral ganglion demonstrated that of the 13 bilateral pairs of cerebral-buccal interneurons in the cerebral ganglion, a subpopulation of 3 are immunopositive for the peptide myomodulin. The present paper describes the properties of two of these cells, which we have termed CBI-8 and CBI-9. CBI-8 and CBI-9 were found to be dye coupled and electrically coupled. The cells have virtually identical properties, and consequently we consider them to be "twin" pairs and refer to them as CBI-8/9. CBI-8/9 were identified by electrophysiological criteria and then labeled with dye. Labeled cells were found to be immunopositive for myomodulin, and, using high pressure liquid chromatography, the cells were shown to contain authentic myomodulin. CBI-8/9 were found to receive synaptic input after mechanical stimulation of the tentacles. They also received excitatory input from C-PR, a neuron involved in neck lengthening, and received a slow inhibitory input from CC5, a cell involved in neck shortening, suggesting that CBI-8/9 may be active during forward movements of the head or buccal mass. Firing of CBI-8 or CBI-9 resulted in the activation of a relatively small number of buccal neurons as evidenced by extracellular recordings from buccal nerves. Firing also produced local movements of the buccal mass, in particular a strong contraction of the I7 muscle, which mediates radula opening. CBI-8/9 were found to produce a slow depolarization and rhythmic activity of B48, the motor neuron for the I7 muscle. The data provide continuing evidence that the small population of cerebral buccal interneurons is composed of neurons that are highly diverse in their functional roles. CBI-8/9 may function as a type of premotor neuron, or perhaps as a peptidergic modulatory neuron, the functions of which are dependent on the coactivity of other neurons. (+info)Regulation of cardiac L-type Ca2+ channel by coexpression of G(alpha s) in Xenopus oocytes. (2/2998)
Activation of G(alpha s) via beta-adrenergic receptors enhances the activity of cardiac voltage-dependent Ca2+ channels of the L-type, mainly via protein kinase A (PKA)-dependent phosphorylation. Contribution of a PKA-independent effect of G(alpha s) has been proposed but remains controversial. We demonstrate that, in Xenopus oocytes, antisense knockdown of endogenous G(alpha s) reduced, whereas coexpression of G(alpha s) enhanced, currents via expressed cardiac L-type channels, independently of the presence of the auxiliary subunits alpha2/delta or beta2A. Coexpression of G(alpha s) did not increase the amount of alpha1C protein in whole oocytes or in the plasma membrane (measured immunochemically). Activation of coexpressed beta2 adrenergic receptors did not cause a detectable enhancement of channel activity; rather, a small cAMP-dependent decrease was observed. We conclude that coexpression of G(alpha s), but not its acute activation via beta-adrenergic receptors, enhances the activity of the cardiac L-type Ca2+ channel via a PKA-independent effect on the alpha1C subunit. (+info)Multidrug resistance (MDR1) P-glycoprotein enhances esterification of plasma membrane cholesterol. (3/2998)
Class I P-glycoproteins (Pgp) confer multidrug resistance in tumors, but the physiologic function of Pgp in normal tissues remains uncertain. In cells derived from tissues that normally express Pgp, recent data suggest a possible role for Pgp in cholesterol trafficking from the plasma membrane to the endoplasmic reticulum. We investigated the esterification of plasma membrane cholesterol under basal conditions and in response to sphingomyelinase treatment in transfected and drug-selected cell lines expressing differing amounts of functional class I Pgp. Compared with parental NIH 3T3 fibroblasts, cells transfected with human multidrug resistance (MDR1) Pgp esterified more cholesterol both without and with sphingomyelinase. Esterification also was greater in drug-selected Dox 6 myeloma cells than parental 8226 cells, which express low and non-immunodetectable amounts of Pgp, respectively. However, no differences in total plasma membrane cholesterol were detected. Transfection of fibroblasts with the multidrug resistance-associated protein (MRP) did not alter esterification, showing that cholesterol trafficking was not generally affected by ATP-binding cassette transporters. Steroidal (progesterone, dehydroepiandrosterone) and non-steroidal antagonists (verapamil, PSC 833, LY335979, and GF120918) were evaluated for effects on both cholesterol trafficking and the net content of 99mTc-Sestamibi, a reporter of drug transport activity mediated by Pgp. In Pgp-expressing cells treated with nonselective and selective inhibitors, both the kinetics and efficacy of inhibition of cholesterol esterification differed from the antagonism of drug transport mediated by Pgp. Thus, although the data show that greater expression of class I Pgp within a given cell type is associated with enhanced esterification of plasma membrane cholesterol in support of a physiologic function for Pgp in facilitating cholesterol trafficking, the molecular mechanism is dissociated from the conventional drug transport activity of Pgp. (+info)Isoforms of the Na-K-2Cl cotransporter in murine TAL II. Functional characterization and activation by cAMP. (4/2998)
The functional properties of alternatively spliced isoforms of the mouse apical Na+-K+-2Cl- cotransporter (mBSC1) were examined, using expression in Xenopus oocytes and measurement of 22Na+ or 86Rb+ uptake. A total of six isoforms, generated by the combinatorial association of three 5' exon cassettes (A, B, and F) with two alternative 3' ends, are expressed in mouse thick ascending limb (TAL) [see companion article, D. B. Mount, A. Baekgaard, A. E. Hall, C. Plata, J. Xu, D. R. Beier, G. Gamba, and S. C. Hebert. Am. J. Physiol. 276 (Renal Physiol. 45): F347-F358, 1999]. The two 3' ends predict COOH-terminal cytoplasmic domains of 129 amino acids (the C4 COOH terminus) and 457 amino acids (the C9 terminus). The three C9 isoforms (mBSC1-A9/F9/B9) all express Na+-K+-2Cl- cotransport activity, whereas C4 isoforms are nonfunctional in Xenopus oocytes. Activation or inhibition of protein kinase A (PKA) does not affect the activity of the C9 isoforms. The coinjection of mBSC1-A4 with mBSC1-F9 reduces tracer uptake, compared with mBSC1-F9 alone, an effect of C4 isoforms that is partially reversed by the addition of cAMP-IBMX to the uptake medium. The inhibitory effect of C4 isoforms is a dose-dependent function of the alternatively spliced COOH terminus. Isoforms with a C4 COOH terminus thus exert a dominant negative effect on Na+-K+-2Cl- cotransport, a property that is reversed by the activation of PKA. This interaction between coexpressed COOH-terminal isoforms of mBSC1 may account for the regulation of Na+-K+-2Cl- cotransport in the mouse TAL by hormones that generate cAMP. (+info)Effects of dauricine, quinidine, and sotalol on action potential duration of papillary muscles in vitro. (5/2998)
AIM: To compare the characteristics of dauricine, sotalol, and quinidine on action potential duration (APD). METHODS: Using intracellular microelectrode method to record APD in guinea pig papillary muscles. RESULTS: Dauricine 20 mumol.L-1 prolonged action potential at 90% repolarization, the percent of APD prolongation were 22 +/- 8, 11 +/- 6, 9 +/- 5, 7 +/- 5, 6 +/- 3, 4.3 +/- 2.8, 4.5 +/- 2.8 at the cycle lengths of 200-2000 ms, dauricine became more effective in lengthening APD at short cycle lengths. The effect of dauricine on prolonging APD exhibited normal use-dependence, whereas quinidine 1 mumol.L-1 and sotalol 10 mumol.L-1 were less effective in lengthening APD at short cycle lengths. The effect of quinidine and sotalol on APD exhibited reverse use-dependence. CONCLUSSION: The effect of dauricine on APD depends on activation frequency. (+info)Protective effect of quinaprilat, an active metabolite of quinapril, on Ca2+-overload induced by lysophosphatidylcholine in isolated rat cardiomyocytes. (6/2998)
We examined the effects of quinaprilat, an active metabolite of quinapril (an angiotensin converting enzyme (ACE) inhibitor) on the increase in intracellular concentration of Ca2+ ([Ca2+]i) (Ca2+-overload) induced by lysophosphatidylcholine (LPC) in isolated rat cardiomyocytes. LPC (15 microM) produced Ca2+-overload with a change in cell-shape from rod to round. Quinaprilat but not quinapril at 20 or 50 microM attenuated the LPC-induced increase in [Ca2+]i and the change in cell-shape in a concentration-dependent manner. Since quinaprilat has an inhibitory action on ACE and quinapril has practically no inhibitory action on ACE, it is likely that the inhibitory action of quinaprilat on ACE is necessary for the protective effect of the drug against LPC-induced changes. We therefore examined the effects of enalapril (another ACE inhibitor with the weak inhibitory action on ACE) and enalaprilat (an active metabolite of enalapril with an inhibitory action on ACE) on the LPC-induced changes. Both enalapril and enalaprilat attenuated the LPC-induced Ca2+-overload, suggesting that the inhibitory action on ACE may not mainly contribute to the protective effect of ACE inhibitors against LPC-induced Ca2+-overload. This suggestion was supported by the fact that neither ACE (0.2 U/ml) nor angiotensin II (0.1-100 microM) increased [Ca2+]i in isolated cardiomyocytes. Furthermore, application of bradykinin (0.01-10 microM) did not enhance the protective effect of quinaprilat against LPC-induced changes. LPC also increased release of creatine kinase (CK) from the myocyte markedly, and quinaprilat but not quinapril attenuated the LPC-induced CK release. Unexpectedly, both enalapril and enalaprilat did not attenuate the LPC-induced CK release. Neither quinapril nor quinaprilat changed the critical micelle concentration of LPC, suggesting that these drugs do not directly bind to LPC. We conclude that quinaprilat attenuates the LPC-induced increase in [Ca2+]i, and that the protective effect of quinaprilat on the LPC-induced change may not be related to a decrease in angiotensin II production or an increase in bradykinin production. (+info)ACE inhibitor versus beta-blocker for the treatment of hypertension in renal allograft recipients. (7/2998)
Angiotensin-converting enzyme (ACE) inhibitors have been shown to slow the progression of chronic renal failure. However, the value of ACE inhibitors for the treatment of hypertension in renal allograft recipients has not been established. ACE inhibitors dilate the efferent glomerular arteriole, an effect that may aggravate the decrease in glomerular filtration rate resulting from cyclosporine-induced vasoconstriction at the afferent glomerular arteriole. Therefore, the goal of this double-blind, randomized study was to compare the antihypertensive and renal effects of the ACE inhibitor quinapril with those of the beta-blocker atenolol in renal allograft recipients in whom hypertension developed 6 to 12 weeks after transplantation. All patients received cyclosporine as an immunosuppressant and had stable graft function (serum creatinine concentration, <220 micromol/L) at entry into the study. Twenty-nine patients who received quinapril (daily dose titrated between 2.5 and 20 mg) and 30 patients who received atenolol (daily dose titrated between 12.5 and 100 mg) completed the 24-month study. The two groups did not differ in age, sex ratio, height, and weight before entry into the study. Quinapril decreased diastolic blood pressure from 96+/-1 to 84+/-1 mm Hg (average throughout treatment period), and atenolol decreased diastolic blood pressure from 96+/-1 to 83+/-1 mm Hg. The serum creatinine concentration did not change significantly in either group after 24 months (129+/-8 micromol/L at entry and 148+/-19 micromol/L after 24 months in the quinapril group and 131+/-6 micromol/L at entry and 152+/-15 micromol/L after 24 months in the atenolol group; P=NS for both groups). After 24 months, the change in urinary albumin excretion from baseline was -10+/-15 mg/d in the quinapril group and 52+/-32 mg/d in the atenolol group (P=0.03). These results show that quinapril and atenolol are effective antihypertensive drugs when used after renal transplantation. Moreover, compared with atenolol, quinapril has no adverse effects on graft function. The relative reduction in albuminuria observed with quinapril as compared with atenolol could indicate a beneficial effect of quinapril on long-term graft function. (+info)Intracellular trafficking pathways in the assembly of connexins into gap junctions. (8/2998)
Trafficking pathways underlying the assembly of connexins into gap junctions were examined using living COS-7 cells expressing a range of connexin-aequorin (Cx-Aeq) chimeras. By measuring the chemiluminescence of the aequorin fusion partner, the translocation of oligomerized connexins from intracellular stores to the plasma membrane was shown to occur at different rates that depended on the connexin isoform. Treatment of COS-7 cells expressing Cx32-Aeq and Cx43-Aeq with brefeldin A inhibited the movement of these chimera to the plasma membrane by 84 +/- 4 and 88 +/- 4%, respectively. Nocodazole treatment of the cells expressing Cx32-Aeq and Cx43-Aeq produced 29 +/- 16 and 4 +/- 7% inhibition, respectively. In contrast, the transport of Cx26 to the plasma membrane, studied using a construct (Cx26/43T-Aeq) in which the short cytoplasmic carboxyl-terminal tail of Cx26 was replaced with the extended carboxyl terminus of Cx43, was inhibited 89 +/- 5% by nocodazole and was minimally affected by exposure of cells to brefeldin A (17 +/-11%). The transfer of Lucifer yellow across gap junctions between cells expressing wild-type Cx32, Cx43, and the corresponding Cx32-Aeq and Cx43-Aeq chimeras was reduced by nocodazole treatment and abolished by brefeldin A treatment. However, the extent of dye coupling between cells expressing wild-type Cx26 or the Cx26/43T-Aeq chimeras was not significantly affected by brefeldin A treatment, but after nocodazole treatment, transfer of dye to neighboring cells was greatly reduced. These contrasting effects of brefeldin A and nocodazole on the trafficking properties and intercellular dye transfer are interpreted to suggest that two pathways contribute to the routing of connexins to the gap junction. (+info)Isoquinolines are not a medical term per se, but a chemical classification. They refer to a class of organic compounds that consist of a benzene ring fused to a piperidine ring. This structure is similar to that of quinoline, but with the nitrogen atom located at a different position in the ring.
Isoquinolines have various biological activities and can be found in some natural products, including certain alkaloids. Some isoquinoline derivatives have been developed as drugs for the treatment of various conditions, such as cardiovascular diseases, neurological disorders, and cancer. However, specific medical definitions related to isoquinolines typically refer to the use or effects of these specific drugs rather than the broader class of compounds.
Sulfur oxides (SOx) are chemical compounds that contain sulfur and oxygen in various oxidation states. The term "sulfur oxides" is often used to refer specifically to sulfur dioxide (SO2) and sulfur trioxide (SO3), which are the most common and widely studied SOx compounds.
Sulfur dioxide is a colorless gas with a sharp, pungent odor. It is produced naturally by volcanic eruptions and is also released into the air when fossil fuels such as coal and oil are burned for electricity generation, industrial processes, and transportation. Exposure to high levels of sulfur dioxide can cause respiratory symptoms such as coughing, wheezing, and shortness of breath.
Sulfur trioxide is a colorless liquid or solid with a pungent, choking odor. It is produced industrially for the manufacture of sulfuric acid and other chemicals. Sulfur trioxide is highly reactive and can cause severe burns and eye damage upon contact.
Both sulfur dioxide and sulfur trioxide contribute to air pollution and have been linked to a range of health and environmental effects, including respiratory problems, acid rain, and damage to crops and forests. As a result, there are regulations in place to limit emissions of these pollutants into the air.
I'm sorry for any confusion, but "Thalictrum" is not a medical term. It is the name of a genus of flowering plants in the family Ranunculaceae, also known as meadow rue. These plants are native to temperate regions of the Northern Hemisphere and have diverse ornamental uses due to their showy flowers. If you have any questions about a medical condition or term, I'd be happy to try to help with that instead!
Cyclization is a chemical process that involves forming a cyclic structure or ring-shaped molecule from a linear or open-chain compound. In the context of medicinal chemistry and drug design, cyclization reactions are often used to synthesize complex molecules, including drugs, by creating rings or fused ring systems within the molecule's structure.
Cyclization can occur through various mechanisms, such as intramolecular nucleophilic substitution, electrophilic addition, or radical reactions. The resulting cyclized compounds may exhibit different chemical and biological properties compared to their linear precursors, making them valuable targets for drug discovery and development.
In some cases, the cyclization process can lead to the formation of stereocenters within the molecule, which can impact its three-dimensional shape and how it interacts with biological targets. Therefore, controlling the stereochemistry during cyclization reactions is crucial in medicinal chemistry to optimize the desired biological activity.
Overall, cyclization plays a significant role in the design and synthesis of many pharmaceutical compounds, enabling the creation of complex structures that can interact specifically with biological targets for therapeutic purposes.
Molecular structure, in the context of biochemistry and molecular biology, refers to the arrangement and organization of atoms and chemical bonds within a molecule. It describes the three-dimensional layout of the constituent elements, including their spatial relationships, bond lengths, and angles. Understanding molecular structure is crucial for elucidating the functions and reactivities of biological macromolecules such as proteins, nucleic acids, lipids, and carbohydrates. Various experimental techniques, like X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and cryo-electron microscopy (cryo-EM), are employed to determine molecular structures at atomic resolution, providing valuable insights into their biological roles and potential therapeutic targets.
Isoquinoline
Isoquinoline alkaloids
Isoquinoline 1-oxidoreductase
Bobbitt reaction
Gigantine
Deoxyepinephrine
Dewan Singh Bhakuni
T. R. Govindachari
Discovery and development of TRPV1 antagonists
Quinoline
Quinaldine
Alexander Shulgin
Piperolactam A
Erysodienone
Pictet-Spengler reaction
Decahydroisoquinoline
Bischler-Napieralski reaction
Β-Carboline
James M. Bobbitt
Combes quinoline synthesis
Duranta erecta
Friedländer synthesis
Doebner-Miller reaction
Magnoflorine
Pfitzinger reaction
Benzylamine
Pomeranz-Fritsch reaction
Isoindole
Carduus crispus
Alkaloid
Isoquinoline - Wikipedia
Isoquinoline, 3-methyl
Plant Poisoning: Quinolizidine and Isoquinoline: Practice Essentials, Pathophysiology, Etiology
IUCr) Crystal structure of 2-methyl-1,2,3,4-tetra-hydro-iso-quinoline trihydrate
Benz[f]isoquinoline, 4-(4-chlorophenyl)-1,2-dihydro- | C19H14ClN | CID 12271871 - PubChem
9,10-Dimethoxy-1'-phenyl-1,3,4,6,7,11b-hexahydro-2'H,5'H-spiro[pyrido[2,1-a]isoquinoline-2,3'-pyrrolidine]-2',5'-dione |...
Isoquinoline
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1H-Benz[de]isoquinoline-1,3(2H)-dione, 6-bromo-2-methyl- | SIELC Technologies
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Synthesis of Isoquinolines by the Pomeranz-Fritsch Reaction - Organic Reactions Wiki
1-(4-TrifluoroMethyl-phenyl)-isoquinoline , - Career Henan Chemical Co.
Buy Chemistry Of Heterocyclic Compounds Isoquinolines Part 3 Volume 38 Second Edition 1995
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Isoquinoline-based Eu(iii) luminescent probes for citrate sensing in complex matrix
EQUIMAX, oral gel/paste for HORSES - VIRBAC - ivermectin + praziquantel, macrocyclic lactone + isoquinoline
Transformations of isocarbostyrils for the synthesis of isoquinoline alkaloids and the related analogues
Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study
Resistance to chemotherapy: new treatments and novel insights into an old problem | British Journal of Cancer
Alkaloids6
- Quinolizidine and isoquinoline are a widely distributed, heterogeneous group of alkaloids with members of each group having known toxicity to humans and domestic animals. (medscape.com)
- Assays for isoquinoline or quinolizidine alkaloids are not routinely available. (medscape.com)
- β-Phenylethylamines and the isoquinoline alkaloids. (novapublishers.com)
- These effects of Rhizoma coptidis are attributed to its alkaloid components, especially isoquinoline alkaloids [ 10 ]. (springer.com)
- We chose five isoquinoline alkaloids (berberine, coptisine, palmatine, jateorrhizine, epiberberine) and one aporphine alkaloid (magnoflorine) of Rhizoma coptidis as research goals (Fig. 1 ). (springer.com)
- b Substituents of the five isoquinoline alkaloids. (springer.com)
Alkaloid2
- Eletefine (1998), an isoquinoline alkaloid Naphthalene, an analog without the nitrogen atom Nomenclature of Organic Chemistry : IUPAC Recommendations and Preferred Names 2013 (Blue Book). (wikipedia.org)
- A practical method for the synthesis of an isoquinoline alkaloid 6,7-dimethoxy-2-methylisoquinoline-1,3,4(2H)-trione and its analogues has been demonstrated. (tcu.edu)
Synthesis2
- In enzymology, the (S)-norcoclaurine synthase (EC 4.2.1.78) is an enzyme that catalyzes a biological Pictect-Spengler synthesis: Intramolecular aza Wittig reactions also afford isoquinolines. (wikipedia.org)
- Synthesis and reactivity of naphthalene, quinolines and isoquinolines. (bath.ac.uk)
Quinoline2
- Isoquinoline and quinoline are benzopyridines, which are composed of a benzene ring fused to a pyridine ring. (wikipedia.org)
- Weissgerber developed a more rapid route in 1914 by selective extraction of coal tar, exploiting the fact that isoquinoline is more basic than quinoline. (wikipedia.org)
Precursors1
- These precursors and dienophiles are based on and drived from isoquinolines and isocarbostyrils. (tcu.edu)
Cyclization1
- the only difference being that an additional hydroxy group in the reactant provides a site for dehydration under the same reaction conditions as the cyclization to give the isoquinoline rather than requiring a separate reaction to convert a dihydroisoquinoline intermediate. (wikipedia.org)
Benz1
- 1H-Benz[de]isoquinoline-1,3(2H)-dione, 6-bromo-2-methyl- can be analyzed by this reverse phase (RP) HPLC method with simple conditions. (sielc.com)
Abstract1
- abstract = "In 4-fluoro-isoquinoline-5-sulfonyl chloride, C9H 5ClFNO2S, (I), one of the two sulfonyl O atoms lies approximately on the isoquinoline plane as a result of minimizing the steric repulsion between the chloro-sulfonyl group and the neighbouring F atom. (elsevierpure.com)
Reactions1
- Two kinds of [3 + 2] cycloaddition intermediates generated from the three-component reactions of 2-bromobenzaldehydes and maleimides with amino esters or amino acids were used for a one-pot N -allylation and intramolecular Heck reactions to form pyrrolidinedione-fused hexahydropyrrolo[2,1- a ]isoquinolines. (beilstein-journals.org)
Derivatives3
- In a broader sense, the term isoquinoline is used to make reference to isoquinoline derivatives. (wikipedia.org)
- Although isoquinoline derivatives can be synthesized by several methods, relatively few direct methods deliver the unsubstituted isoquinoline. (wikipedia.org)
- Several other methods are useful for the preparation of various isoquinoline derivatives. (wikipedia.org)
Method2
- The Pomeranz-Fritsch reaction provides an efficient method for the preparation of isoquinoline. (wikipedia.org)
- The melting point determination of 2-octadecyl-1H-thioxantheno[2,1,9-def]isoquinoline- 1,3(2H)-dione (CAS No. 27870-92-4) was done following OECD Guideline 102 and according to the metal block capillary method. (europa.eu)
Natural1
- The isoquinoline ring in these natural compound derives from the aromatic amino acid tyrosine. (wikipedia.org)
Tyrosine1
- The isoquinoline ring in these natural compound derives from the aromatic amino acid tyrosine. (wikipedia.org)
Potent1
- Amino group-substituted compounds, especially 5-piperazinyl indeno[1,2-c]isoquinoline 7f, displayed potent topoisomerase I inhibitory activity as well as cytotoxicities against five different tumor cell lines. (ewha.ac.kr)
Chemical1
- Wego Chemical Group is a long-experienced distributor of Isoquinoline. (wegochem.com)
Aromatic1
- Isoquinoline is a heterocyclic aromatic organic compound. (wikipedia.org)
Chemistry1
- Eletefine (1998), an isoquinoline alkaloid Naphthalene, an analog without the nitrogen atom Nomenclature of Organic Chemistry : IUPAC Recommendations and Preferred Names 2013 (Blue Book). (wikipedia.org)
Type1
- To evaluate these interactions during chronic administration, we treated mice with lorazepam for 1 to 14 days alone or in combination with the peripheral-type site ligand PK11195 [N-methyl-N-(methyl-1-propyl)chloro-2-phenyl-1-isoquinoline-3-carboxamid e]. (nih.gov)
Structure1
- The structure-aided and cell-based structure-activity relationship studies on a series of tetrahydro-isoquinolines lead to efficient discovery of a qualified lead compound (16) with the high potency and selectivity, well-characterized binding mechanism, high cell permeability, good safety and pharmacokinetic profile, and impressive in vivo efficacy on antipsoriasis, in particular with a topical application. (rcsb.org)
Efficient1
- The Pomeranz-Fritsch reaction provides an efficient method for the preparation of isoquinoline. (wikipedia.org)