An ionophorous, polyether antibiotic from Streptomyces chartreusensis. It binds and transports CALCIUM and other divalent cations across membranes and uncouples oxidative phosphorylation while inhibiting ATPase of rat liver mitochondria. The substance is used mostly as a biochemical tool to study the role of divalent cations in various biological systems.
ISOQUINOLINES with a benzyl substituent.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.

Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model. (1/3227)

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

Relaxation of endothelin-1-induced pulmonary arterial constriction by niflumic acid and NPPB: mechanism(s) independent of chloride channel block. (2/3227)

We investigated the effects of the Cl- channel blockers niflumic acid, 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) and 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) on endothelin-1 (ET-1)-induced constriction of rat small pulmonary arteries (diameter 100-400 microm) in vitro, following endothelium removal. ET-1 (30 nM) induced a sustained constriction of rat pulmonary arteries in physiological salt solution. Arteries preconstricted with ET-1 were relaxed by niflumic acid (IC50: 35.8 microM) and NPPB (IC50: 21.1 microM) in a reversible and concentration-dependent manner. However, at concentrations known to block Ca++-activated Cl- channels, DIDS (+info)

Oxygen-dependent K+ influxes in Mg2+-clamped equine red blood cells. (3/3227)

1. Cl--dependent K+ (86Rb+) influxes were measured in oxygenated and deoxygenated equine red blood cells, whose free [Mg2+]i had been clamped, to examine the effect on O2 dependency of the K+-Cl- cotransporter. 2. Total [Mg2+]i was 2.55 +/- 0.07 mM (mean +/- s.e.m. , n = 6). Free [Mg2+]i was estimated at 0.45 +/- 0.04 and 0.68 +/- 0. 03 mM (mean +/- s.e.m., n = 4) in oxygenated and deoxygenated red cells, respectively. 3. K+-Cl- cotransport was minimal in deoxygenated cells but substantial in oxygenated ones. Cl--dependent K+ influx, inhibited by calyculin A, consistent with mediation via the K+-Cl- cotransporter, was revealed by depleting deoxygenated cells of Mg2+. 4. Decreasing [Mg2+]i stimulated K+ influx, and increasing [Mg2+]i inhibited it, in both oxygenated and deoxygenated red cells. When free [Mg2+]i was clamped, Cl--dependent K+ influxes were always greater in oxygenated cells than in deoxygenated ones, and changes in free [Mg2+]i of the magnitude occurring during oxygenation-deoxygenation cycles had a minimal effect. Physiological fluctuations in free [Mg2+]i are unlikely to provide the primary link coupling activity of the K+-Cl- cotransporter with O2 tension. 5. Volume and H+ ion sensitivity of K+ influx in Mg2+-clamped red cells were increased in O2 compared with those in deoxygenated cells at the same free [Mg2+]i, by about 6- and 2-fold, respectively, but again these features were not responsible for the higher fluxes in oxygenated cells. 6. Regulation of the K+-Cl- cotransporter by O2 is very similar in equine, sheep and in normal human (HbA) red cells, but altered in human sickle cells. Present results imply that, as in sheep red cells, O2 dependence of K+-Cl- cotransport in equine red cells is not mediated via changes in free [Mg2+]i and that cotransport in Mg2+-clamped red cells is still stimulated by O2. This behaviour is contrary to that reported for human sickle (HbS) cells.  (+info)

Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve. (4/3227)

1. Using a microelectrode technique, acetylcholine (ACh)-induced membrane potential changes were characterized using various types of inhibitors of K+ and Cl- channels in rabbit aortic valve endothelial cells (RAVEC). 2. ACh produced transient then sustained membrane hyperpolarizations. Withdrawal of ACh evoked a transient depolarization. 3. High K+ blocked and low K+ potentiated the two ACh-induced hyperpolarizations. Charybdotoxin (ChTX) attenuated the ACh-induced transient and sustained hyperpolarizations; apamin inhibited only the sustained hyperpolarization. In the combined presence of ChTX and apamin, ACh produced a depolarization. 4. In Ca2+-free solution or in the presence of Co2+ or Ni2+, ACh produced a transient hyperpolarization followed by a depolarization. In BAPTA-AM-treated cells, ACh produced only a depolarization. 5. A low concentration of A23187 attenuated the ACh-induced transient, but not the sustained, hyperpolarization. In the presence of cyclopiazonic acid, the hyperpolarization induced by ACh was maintained after ACh removal; this maintained hyperpolarization was blocked by Co2+. 6. Both NPPB and hypertonic solution inhibited the membrane depolarization seen after ACh washout. Bumetanide also attenuated this depolarization. 7. It is concluded that in RAVEC, ACh produces a two-component hyperpolarization followed by a depolarization. It is suggested that ACh-induced Ca2+ release from the storage sites causes a transient hyperpolarization due to activation of ChTX-sensitive K+ channels and that ACh-activated Ca2+ influx causes a sustained hyperpolarization by activating both ChTX- and apamin-sensitive K+ channels. Both volume-sensitive Cl- channels and the Na+-K+-Cl- cotransporter probably contribute to the ACh-induced depolarization.  (+info)

The cyclo-oxygenase-dependent regulation of rabbit vein contraction: evidence for a prostaglandin E2-mediated relaxation. (5/3227)

1. Arachidonic acid (0.01-1 microM) induced relaxation of precontracted rings of rabbit saphenous vein, which was counteracted by contraction at concentrations higher than 1 microM. Concentrations higher than 1 microM were required to induce dose-dependent contraction of vena cava and thoracic aorta from the same animals. 2. Pretreatment with a TP receptor antagonist (GR32191B or SQ29548, 3 microM) potentiated the relaxant effect in the saphenous vein, revealed a vasorelaxant component in the vena cava response and did not affect the response of the aorta. 3. Removal of the endothelium from the venous rings, caused a 10 fold rightward shift in the concentration-relaxation curves to arachidonic acid. Whether or not the endothelium was present, the arachidonic acid-induced relaxations were prevented by indomethacin (10 microM) pretreatment. 4. In the saphenous vein, PGE2 was respectively a 50 and 100 fold more potent relaxant prostaglandin than PGI2 and PGD2. Pretreatment with the EP4 receptor antagonist, AH23848B, shifted the concentration-relaxation curves of this tissue to arachidonic acid in a dose-dependent manner. 5. In the presence of 1 microM arachidonic acid, venous rings produced 8-10 fold more PGE2 than did aorta whereas 6keto-PGF1alpha and TXB2 productions remained comparable. 6. Intact rings of saphenous vein relaxed in response to A23187. Pretreatment with L-NAME (100 microM) or indomethacin (10 microM) reduced this response by 50% whereas concomitant pretreatment totally suppressed it. After endothelium removal, the remaining relaxing response to A23187 was prevented by indomethacin but not affected by L-NAME. 7. We conclude that stimulation of the cyclo-oxygenase pathway by arachidonic acid induced endothelium-dependent, PGE2/EP4 mediated relaxation of the rabbit saphenous vein. This process might participate in the A23187-induced relaxation of the saphenous vein and account for a relaxing component in the response of the vena cava to arachidonic acid. It was not observed in thoracic aorta because of the lack of a vasodilatory receptor and/or the poorer ability of this tissue than veins to produce PGE2.  (+info)

Differences in the actions of some blockers of the calcium-activated potassium permeability in mammalian red cells. (6/3227)

1. The actions of some inhibitors of the Ca2+-activated K+ permeability in mammalian red cells have been compared. 2. Block of the permeability was assessed from the reduction in the net loss of K+ that followed the application of the Ca2+ ionophore A23187 (2 microM) to rabbit red cells suspended at a haematocrit of 1% in a low potassium solution ([K]0 0.12-0.17 mM) at 37 degrees C. Net movement of K+ was measured using a K+-sensitive electrode placed in the suspension. 3. The concentrations (microM +/- s.d.) of the compounds tested causing 50% inhibition of K+ loss were: quinine, 37 +/- 3; cetiedil, 26 +/- 1; the cetiedil congeners UCL 1269, UCL 1274 and UCL 1495, approximately 150, 8.2 +/- 0.1, 0.92 +/- 0.03 respectively; clotrimazole, 1.2 +/- 0.1; nitrendipine, 3.6 +/- 0.5 and charybdotoxin, 0.015 +/- 0.002. 4. The characteristics of the block suggested that compounds could be placed in two groups. For one set (quinine, cetiedil, and the UCL congeners), the concentration-inhibition curves were steeper (Hill coefficient, nH, > or = 2.7) than for the other (clotrimazole, nitrendipine, charybdotoxin) for which nH approximately 1. 5. Compounds in the first set alone became less active on raising the concentration of K+ in the external solution to 5.4 mM. 6. The rate of K+ loss induced by A23187 slowed in the presence of high concentrations of cetiedil and its analogues, suggesting a use-dependent component to the inhibitory action. This was not seen with clotrimazole. 7. The blocking action of the cetiedil analogue UCL 1274 could not be overcome by an increase in external Ca2+ and its potency was unaltered when K+ loss was induced by the application of Pb2+ (10 microM) rather than by A23187. 8. These results, taken with the findings of others, suggest that agents that block the red cell Ca2+-activated K+ permeability can be placed in two groups with different mechanisms of action. The differences can be explained by supposing that clotrimazole and charybdotoxin act at the outer face of the channel whereas cetiedil and its congeners may block within it, either at or near the K+ binding site that determines the flow of K+.  (+info)

Arterial flow conditions downregulate thrombomodulin on saphenous vein endothelium. (7/3227)

BACKGROUND: The antithrombogenic properties of venous endothelium may be attenuated when vein is implanted in the arterial circulation. Such changes may facilitate thrombosis, which is the final common pathway for saphenous vein arterial bypass graft occlusion. METHODS AND RESULTS: Using human saphenous vein in a validated ex vivo flow circuit, we investigated (1) the possibility that arterial flow conditions (mean pressure, 100 mm Hg, 90 cpm, approximately 200 mL/min) alter the concentration of proteins involved in regulating thrombosis at the vessel wall and (2) the influence of ion channel blockade on such effects. Concentrations of thrombomodulin and tissue factor were quantified by Western blotting (ratio of von Willebrand factor staining) and immunohistochemistry (as a percentage of CD31-staining area). Thrombomodulin concentrations after 90 minutes of venous and arterial flow conditions were quantified by immunostaining (68.9+/-4.8% and 41.0+/-3.0% CD31, respectively; P<0.01) and by Western blotting (1.35+/-0.20 and 0. 15+/-0.03 ratio of von Willebrand factor, respectively; P<0.01). The ability of endothelial cells to generate activated protein C also decreased from 62+/-14 to 19+/-10 ng. min-1. 1000 cells-1 (P=0.01). The significant reduction in thrombomodulin was attenuated if calcium was removed from the perfusate but not by external vein stenting. Inclusion in the vein perfusate of drugs that reduce calcium entry (including Gd3+, to block stretch-activated ion channels, and nifedipine) abolished the reduction in thrombomodulin concentration observed after arterial flow conditions. In freshly excised vein, negligible concentrations of tissue factor were detected on the endothelium and concentrations did not increase after 90 minutes of arterial flow conditions, although the inclusion of nifedipine caused the immunostaining to increase from 3.0+/-0.4% to 8.5+/-0.7% CD31 (P<0.02). CONCLUSIONS: In saphenous vein endothelium exposed to arterial flow conditions, there is rapid downregulation of thrombomodulin, sufficient to limit protein C activation, by a calcium-dependent mechanism.  (+info)

Bcl-2 alters the balance between apoptosis and necrosis, but does not prevent cell death induced by oxidized low density lipoproteins. (8/3227)

Oxidized low density lipoproteins (oxLDL) participate in atherosclerosis plaque formation, rupture, and subsequent thrombosis. Because oxLDL are toxic to cultured cells and Bcl-2 protein prevents apoptosis, the present work aimed to study whether Bcl-2 may counterbalance the toxicity of oxLDL. Two experimental model systems were used in which Bcl-2 levels were modulated: 1) lymphocytes in which the (high) basal level of Bcl-2 was reduced by antisense oligonucleotides; 2) HL60 and HL60/B (transduced by Bcl-2) expressing low and high Bcl-2 levels, respectively. In cells expressing relatively high Bcl-2 levels (lymphocytes and HL60/B), oxLDL induced mainly primary necrosis. In cells expressing low Bcl-2 levels (antisense-treated lymphocytes, HL60 and ECV-304 endothelial cells), the rate of oxLDL-induced apoptosis was higher than that of primary necrosis. OxLDL evoked a sustained calcium rise, which is a common trigger to necrosis and apoptosis since both types of cell death were blocked by the calcium chelator EGTA. Conversely, a sustained calcium influx elicited by the calcium ionophore A23187 induced necrosis in cells expressing high Bcl-2 levels and apoptosis in cells expressing low Bcl-2 levels. This suggests that Bcl-2 acts downstream from the calcium peak and inhibits only the apoptotic pathway, not the necrosis pathway, thus explaining the apparent shift from oxLDL-induced apoptosis toward necrosis when Bcl-2 is overexpressed.  (+info)

Calcimycin is a ionophore compound that is produced by the bacterium Streptomyces chartreusensis. It is also known as Calcineurin A inhibitor because it can bind to and inhibit the activity of calcineurin, a protein phosphatase. In medical research, calcimycin is often used to study calcium signaling in cells.
It has been also used in laboratory studies for its antiproliferative and pro-apoptotic effects on certain types of cancer cells. However, it is not approved for use as a drug in humans.

Benzylisoquinolines are a type of naturally occurring organic compounds found in various plants. These compounds are derived from the combination of a benzyl group and an isoquinoline ring, hence the name "benzylisoquinolines." They are known to have diverse biological activities, including anti-inflammatory, antispasmodic, and antimicrobial properties. Some well-known examples of benzylisoquinoline alkaloids include papaverine, found in the opium poppy, and berberine, found in various medicinal plants such as goldenseal and barberry. These compounds have been used in traditional medicine for centuries and continue to be studied for their potential therapeutic uses.

Calcium is an essential mineral that is vital for various physiological processes in the human body. The medical definition of calcium is as follows:

Calcium (Ca2+) is a crucial cation and the most abundant mineral in the human body, with approximately 99% of it found in bones and teeth. It plays a vital role in maintaining structural integrity, nerve impulse transmission, muscle contraction, hormonal secretion, blood coagulation, and enzyme activation.

Calcium homeostasis is tightly regulated through the interplay of several hormones, including parathyroid hormone (PTH), calcitonin, and vitamin D. Dietary calcium intake, absorption, and excretion are also critical factors in maintaining optimal calcium levels in the body.

Hypocalcemia refers to low serum calcium levels, while hypercalcemia indicates high serum calcium levels. Both conditions can have detrimental effects on various organ systems and require medical intervention to correct.

... is also known as Calcimycin, Calcium Ionophore, Antibiotic A23187 and Calcium Ionophore A23187. It is produced at ... a vendor's product page Calcimycin from Bioaustralis, a vendor's product page (Webarchive template wayback links, Articles with ... "Characterization of the biosynthesis gene cluster for the pyrrole polyether antibiotic calcimycin (A23187) in Streptomyces ...
... calcimycin MeSH D03.438.221.346 - chlorzoxazone MeSH D03.438.221.370 - cialit MeSH D03.438.221.950 - zoxazolamine MeSH D03.438. ...
Transportan Family 2.B.11 The Calcimycin or A23187 Carrier-type Ionophore Family 2.B.12 The Salinomycin Family 2.B.13 The ...
Azide Biguanides Bupivacaine Calcimycin (A23187) Dodecyltriphenylphosphonium (C12TPP) Lasalocid (X537A) Long-chain fatty acids ...
Calcimycin, Calcium Ionophore) Abamectine Abietic acid Acetic acid Acetylcholine Actin Actinomycin D Adenine Adenosmeme ...
A23187 is also known as Calcimycin, Calcium Ionophore, Antibiotic A23187 and Calcium Ionophore A23187. It is produced at ... a vendors product page Calcimycin from Bioaustralis, a vendors product page (Webarchive template wayback links, Articles with ... "Characterization of the biosynthesis gene cluster for the pyrrole polyether antibiotic calcimycin (A23187) in Streptomyces ...
Calcimycin. Description. A mobile ion-carrier that forms stable complexes with divalent cations. Useful for increasing ...
Calcimycin Suppresses S100A4 Expression and Inhibits the Stimulatory Effect of Transforming Growth Factor β1 on Keloid ...
A-23187, also known as Calcimycin or Calcium Ionophore III, is a calcium ionophore that rapidly equilibrates intracellular and ... A-23187, also known as Calcimycin or Calcium Ionophore III, is a calcium ionophore that rapidly equilibrates intracellular and ...
A23187 (Calcimycin) has an intrinsic fluorescence excitable by UV light, making it less useful with UV-excitable Ca2+ ...
It can be produced synthetically but is also found in bioactive natural products like nataxazole, caboxamycin and calcimycin. ...
... calcium ionophore calcimycin (A23187), staurosporine (STS), N-methyl-D-aspartate (NMDA), and Maitotoxin (MTX)) that mimic ...
Inhibition of release of prostaglandins and leukotrienes from calcimycin-induced mouse peritoneal macrophages and bovine aorta ...
2000) A second study, involving the chemotherapy drugs etoposide and calcimycin, confirms this finding: Human Burkitts ...
Calcimycin Medicine & Life Sciences 33% * Oxalate(2-) Chemical Compounds 26% * Pentadecanoic Acid Chemical Compounds 25% ...
Example for the four fields above: Calcimycin. *Previous Indexing: free text field that refers to descriptors or descriptor/ ...
Dive into the research topics of Oxygen modulates nitric oxide production selectively in fetal pulmonary endothelial cells.. Together they form a unique fingerprint. ...
Yamashita, T., Ono, K., Ohuchi, H., Yumoto, A., Gotoh, H., Tomonari, S., Sakai, K., Fujita, H., Imamoto, Y., Noji, S., Nakamura, K. & Shichida, Y., Feb 14 2014, In: Journal of Biological Chemistry. 289, 7, p. 3991-4000 10 p.. Research output: Contribution to journal › Article › peer-review ...
Dive into the research topics of Identification of a 57-kilodalton selenoprotein in human thyrocytes as thioredoxin reductase and evidence that its expression is regulated through the calcium-phosphoinositol signaling pathway. Together they form a unique fingerprint. ...
Dive into the research topics of Effects of the incubation of long-chain polyunsaturated fatty acids on platelet lipids and thromboxane release. Together they form a unique fingerprint. ...
HRP, horseradish peroxidase; IBMX, 3-isobutyl-1-methylxanthine; ICI 182,780, fulvestrant; A-23187, calcimycin.. Machado et al. ... calcimycin), sug- (fulvestrant). Our data suggest the presence of membrane gesting that estrogens did not directly act on the ...
Calcimycin Medicine & Life Sciences 82% * Cholesterol Medicine & Life Sciences 74% * Ferredoxin-NADP Reductase Medicine & Life ...
Mixed Calcium-Magnesium salt of A23187 (Calcimycin) is prepared chemically from A23187 (Calcimycin... ... A23187 (Calcimycin) is mobile ion-carrier that forms stable complexes with divalent cations. This... ... Brominated Analog of A23187 (Calcimycin). A23187 is an ionophore antibiotic that forms dimeric... ...
There is also a significant positive correlation between calcimycin and secondary bile acids. Lactiplantibacillus plantarum ... The content of the bacterial metabolite Calcimycin increases. Annotations of metabolic pathways suggest that ... Microbiota-metabolite correlation analysis reveals a significant negative correlation between calcimycin and Lactonacillus and ... a significant positive correlation between calcimycin and Shigella. ...
Many natural compounds of antibiotic nature such as valinomycin [1], streptogramins (group B) [2] and calcimycin [3] exhibit ...
... "calcimycin" EXACT [] xref: CHEBI:3305 xref: MESH:D000001 xref: PMID:22508433 is_a: XCO:0000140 ! vasodilator created_by: ...
Mawatwal S, Behura A, Ghosh A, Kidwai S, Mishra A, Deep A, Agarwal S, Saha S, Singh R and Dhiman R. Calcimycin mediates ... Mawatwal, S., Behura A., Mishra A., Singh R., and Dhiman R. Calcimycin induced IL-12 production inhibits intracellular ... ESAT-6 modulates Calcimycin-induced autophagy through microRNA-30a in mycobacteria infected macrophages. Journal of Infection ... ESAT-6 imepedes IL-18 mediated phagosome lysosome fusion via microRNA-30a upon Calcimycin treatment in mycobacteria infected ...
Calcimycin, Spectrin, Fluorescent Antibody Technique ...
Under the supervision of Robert K. Boeckman Jr., he completed the total synthesis of the ionophore calcimycin, which earned him ...
Li W-C, Kuszak JR, Wang G-M, Wu Z-Q, Abraham S. Calcimycin-induced lens epithelial cell apoptosis contributes to cataract ...
Calcimycin D3.438.221.173 D3.633.100.221.173 Calcitonin D12.776.641.650.95 D12.776.631.650.95 Calcitonin Gene-Related Peptide ...
Calcimycin D3.438.221.173 D3.633.100.221.173 Calcitonin D12.776.641.650.95 D12.776.631.650.95 Calcitonin Gene-Related Peptide ...
Calcimycin D3.438.221.173 D3.633.100.221.173 Calcitonin D12.776.641.650.95 D12.776.631.650.95 Calcitonin Gene-Related Peptide ...
Calcimycin D3.438.221.173 D3.633.100.221.173 Calcitonin D12.776.641.650.95 D12.776.631.650.95 Calcitonin Gene-Related Peptide ...
  • A23187 is also known as Calcimycin, Calcium Ionophore, Antibiotic A23187 and Calcium Ionophore A23187. (wikipedia.org)
  • A-23187, also known as Calcimycin or Calcium Ionophore III, is a calcium ionophore that rapidly equilibrates intracellular and extracellular calcium concentrations. (biotium.com)
  • However, these agents failed to modify the secretion elicited by high Ca2ϩ in nanomolar concentrations of the antiestrogen ICI 182,780 glands treated with the ionophore A-23187 (calcimycin), sug- (fulvestrant). (drugstodaypdf.com)
  • Under the supervision of Robert K. Boeckman Jr., he completed the total synthesis of the ionophore calcimycin, which earned him the degrees of M.Sc. (charettelab.ca)
  • A23187 (Calcimycin) has an intrinsic fluorescence excitable by UV light, making it less useful with UV-excitable Ca 2 + indicators, e.g. (abcam.com)
  • Mixed Calcium-Magnesium salt of A23187 (Calcimycin) is prepared chemically from A23187 (Calcimycin. (fermentek.com)
  • A23187 (Calcimycin) is mobile ion-carrier that forms stable complexes with divalent cations. (fermentek.com)
  • Brominated Analog of A23187 (Calcimycin). (fermentek.com)