
Bioorganic & Medicinal Chemistry
Keywords: Synthesis. New drug molecules. New chemical entities. Medicine …Degarelix acetate (Firmagon®) . ….. Scheme 5. Synthesis of degarelix acetate (V).
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In experiments with mice, Johns Hopkins Kimmel Cancer Center scientists have identified an enzyme involved in the regulation of immune system T cells that could be a useful target in treating asthma and boosting the effects of certain cancer therapies.
In research described online April 6 in Nature Immunology, the investigators show that mice without the enzyme SKG1 were resistant to dust mite-induced asthma. And mice with melanoma and missing the enzyme, developed far fewer lung tumors—less than half as many—than mice with SKG1.
“If we can develop a drug that blocks the enzyme in a way that mimics what happens when the enzyme is missing, we would not only have a treatment to inhibit asthma, but also a drug that could be used in conjunction with other experimental therapies aimed at helping the immune system fight cancer,” said Jonathan D. Powell, M.D., professor of oncology at the…
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Degarelix
214766-78-6 CAS
Degarelix is used for the treatment of advanced prostate cancer. Degarelix is a synthetic peptide derivative drug which binds to gonadotropin-releasing hormone (GnRH) receptors in the pituitary gland and blocks interaction with GnRH. This antagonism reduces luteinising hormone (LH) and follicle-stimulating hormone (FSH) which ultimately causes testosterone suppression. Reduction in testosterone is important in treating men with advanced prostate cancer. Chemically, it is a synthetic linear decapeptide amide with seven unnatural amino acids, five of which are D-amino acids. FDA approved on December 24, 2008.
A subgroup of patients with advanced prostate cancer could now get access to a new treatment option in England and Wales after cost regulators for the NHS issued a green light for Ferring’s Firmagon (degarelix).
In final draft guidance published this morning by the National Institute for Health and Care Excellence, the drug has been recommended as an option for treating advanced hormone-dependent prostate cancer but specifically in patients with spinal metastases who present with signs or symptoms of spinal cord compression.
Read more at: http://www.pharmatimes.com/Article/14-04-15/NICE_nod_for_Firmagon_s_prostate_cancer_drug.aspx#ixzz2z6tthLDT
Carin WINDERSTROM, “KIT AND METHOD FOR PREPARATION OF A DEGARELIX SOLUTION.” U.S. Patent US20100286603, issued November 11, 2010.
FIRMAGON is a sterile lyophilized powder for injection containing degarelix (as the acetate) and mannitol. Degarelix is a synthetic linear decapeptide amide containing seven unnatural amino acids, five of which are D-amino acids. The acetate salt of degarelix is a white to off-white amorphous powder of low density as obtained after lyophilization.
The chemical name of degarelix is D-Alaninamide, N-acetyl-3-(2-naphthalenyl)-D-alanyl-4-chloro-Dphenylalanyl-3-(3-pyridinyl)-D-alanyl-L-seryl-4-[[[(4S)-hexahydro-2,6-dioxo-4pyrimidinyl]carbonyl]amino]-L phenylalanyl-4-[(aminocarbonyl)amino]-D-phenylalanyl-L leucyl-N6–(1-methylethyl)-L-lysyl-L-prolyl. It has an empirical formula of C82H103N18O16Cl and a molecular weight of 1632.3 Da.
Degarelix has the following structural formula:
FIRMAGON delivers degarelix acetate, equivalent to 120 mg of degarelix for the starting dose, and 80 mg of degarelix for the maintenance dose. The 80 mg vial contains 200 mg mannitol and the 120 mg vial contains 150 mg mannitol.
Degarelix (INN) or degarelix acetate (USAN) (tradename Firmagon) is a hormonal therapy used in the treatment of prostate cancer. During development it was known as FE200486.
Testosterone is a male hormone that promotes growth of many prostate tumours and therefore reducing circulating testosterone to very low (castration) levels is often the treatment goal in the management of men with advanced prostate cancer. Degarelix has an immediate onset of action, binding to gonadotropin-releasing hormone (GnRH) receptors in the pituitary gland and blocking their interaction with GnRH. This induces a fast and profound reduction in luteinising hormone (LH), follicle-stimulating hormone (FSH) and in turn, testosterone suppression.[1]
On 24 December 2008, the Food and Drug Administration (FDA) approved degarelix for the treatment of patients with advanced prostate cancer in the USA.[2] It was subsequently approved by the European Commission at the recommendation of the European Medicines Agency (EMEA) on February 17, 2009 for use in adult male patients with advanced, hormone-dependent prostate cancer.Ferring Pharmaceuticals markets the drug under the name Firmagon.
GnRH antagonists (receptor blockers) such as degarelix are a new type of hormonal therapy for prostate cancer. These agents are synthetic peptide derivatives of the natural GnRH decapeptide – a hormone that is made by neurons in the hypothalamus. GnRH antagonists compete with natural GnRH for binding to GnRH receptors in the pituitary gland. This reversible binding blocks the release of LH and FSH from the pituitary. The reduction in LH subsequently leads to a rapid and sustained suppression of testosterone release from the testes and subsequently reduces the size and growth of the prostate cancer. This in turn results in a reduction in prostate-specific antigen (PSA) levels in the patient’s blood. Measuring PSA levels is a way to monitor how patients with prostate cancer are responding to treatment.
Unlike the GnRH agonists, which cause an initial stimulation of the hypothalamic-pituitary-gonadal axis (HPGA), leading to a surge in testosterone levels, and under certain circumstances, a flare-up of the tumour, GnRH antagonists do not cause a surge in testosterone or clinical flare.[3] Clinical flare is a phenomenon that occurs in patients with advanced disease, which can precipitate a range of clinical symptoms such as bone pain, urethral obstruction, and spinal cord compression. Drug agencies have issued boxed warnings regarding this phenomenon in the prescribing information for GnRH agonists. As testosterone surge does not occur with GnRH antagonists, there is no need for patients to receive an antiandrogen as flare protection during prostate cancer treatment. GnRH agonists also induce an increase in testosterone levels after each reinjection of the drug – a phenomenon that does not occur with GnRH antagonists such as degarelix.
GnRH antagonists have an immediate onset of action leading to a fast and profound suppression of testosterone and are therefore especially valuable in the treatment of patients with prostate cancer where fast control of disease is needed.
A Phase III, randomised, 12 month clinical trial (CS21) in prostate cancer[4] compared androgen deprivation with one of two doses of degarelix or the GnRH agonist, leuprolide. Both degarelix doses were at least as effective as leuprolide at suppressing testosterone to castration levels (≤0.5 ng/mL) from Day 28 to study end (Day 364). Testosterone levels were suppressed significantly faster with degarelix than with leuprolide, with degarelix uniformly achieving castration levels by Day 3 of treatment which was not seen in the leuprolide group. There were no testosterone surges with degarelix compared with surges in 81% of those who received leuprolide. Degarelix resulted in a faster reduction in PSA levels compared with leuprolide indicating faster control of the prostate cancer. Recent results also suggest that degarelix therapy may result in longer control of prostate cancer compared with leuprolide.[5]
As with all hormonal therapies, degarelix is commonly associated with hormonal side effects such as hot flashes and weight gain.[4][6][7] Due to its mode of administration (subcutaneous injection), degarelix is also associated with injection-site reactions such as injection-site pain, erythema or swelling. Injection-site reactions are usually mild or moderate in intensity and occur predominantly after the first dose, decreasing in frequency thereafter.[4]
FSH receptors are selectively expressed on the luminal surface of the blood vessels of a wide range of tumors.[8] There may be a potential role for suppression of FSH or FSH receptors. This work is in early stages. It is thought that FSH receptors are important in tumor angiogenesis by signalling via two pathways, one involving VEGF, and a Gq/11mechanism that activates VEGFR-2 independently of VEGF.[8]

Keywords: Synthesis. New drug molecules. New chemical entities. Medicine …Degarelix acetate (Firmagon®) . ….. Scheme 5. Synthesis of degarelix acetate (V).
………………………………
http://www.google.com/patents/US20120041172
Example 1
Hydantoin formation in the synthesis of degarelix. The rearrangement of the hydroorotic group to a hydantoinacetyl group in the production of degarelix has been seen at two stages and two sets of basic conditions.
The first rearrangement appeared during basic extractions of the segment Z-Ser(tBu)-4Aph(Hor)-D-4Aph(tBu-Cbm)-Leu-ILys(Boc)-Pro-D-Ala-NH2. The pH was adjusted to 9.1 in the organic/aqueous two-phase system using conc. NaOH solution, resulting in the formation of 4.5% by weight of the hydantoin analogue. The mechanism appeared to comprise two steps: (a) hydrolysis of the 6-membered hydroorotic moiety under basic conditions followed by ring closure to the 5-membered hydantoin analogue under acidic conditions.
The second rearrangement was observed during evaporation of the segment Z-Ser(tBu)-4Aph(Hor)-D-4Aph(tBu-Cbm)-Leu-OH.DCHA. After the preceding extractions, Z-Ser(tBu)-4Aph(Hor)-D-4Aph(tBu-Cbm)-Leu-OH was dissolved in a mixture of ethyl acetate and 2-butanol. DCHA (2.5 eq.) was added because the segment is isolated as the DCHA salt after evaporation of the solvent followed by a precipitation step. In the particular batch both the hydantoin analogue and the hydrolysed form (mentioned above) were identified. Quantification of the hydantoin was not possible because poor separation by HPLC from other products; the hydrolyzed form was formed in an amount of 1.34% by weight of the combined products. Experimental evidence showed that the amount of rearrangement/hydrolysis was related to the amount of DCHA used in the method.
The following experiment provided further proof of the instability of the hydrooroic moiety under basic conditions. Z-Ser(tBu)-4Aph(Hor)-D-4Aph(tBu-Cbm)-Leu-OH.DCHA (67 mM) was dissolved in wet 2-BuOH with 167 mM (2.5 eq) DCHA at 31° C. After 25 h, 1.3% of the hydantoin analogue and 0.3% of the hydrolysed intermediate had been formed.
Example 2
Stability of degarelix in DBU/DMF and piperidine/DMF. The stability of degarelix was tested under conditions corresponding to those used for removal of the Fmoc-group during SPPS. The hydroorotic group in the side chain of 4Aph(Hor), amino acid residue no. 5 in the sequence of degarelix, is known to be sensitive to base and rearrange to a hydantoinacetyl group. All SPPS procedures known to the inventors had been based on Boc-chemistry.
Samples of degarelix were dissolved in 20% piperidine/DMF; 2% DBU in DMF, and 2% DBU+5% water in DMF; respectively. The samples were analysed by HPLC after 20 h and the amount of the hydantoin analogue determined.
2% DBU/DMF resulted in the formation of 1.8% hydantoin. If 5% water was present, too (simulating wet DMF), the amount was increased to 7%. Surprisingly, the use of 20% piperidine in DMF did not result in any formation of the hydantoin analogue, indicating that this mixture might be useful for Fmoc-based SPPS of Degarelix.
Example 3 Synthesis and Purification of Degarelix Using Fmo-/Rink Amide AM Resin
Step 1. Fmoc-Rink amide AM resin (64 g; substitution 0.67 mmol/g) was placed in a reactor and washed with 1.9 L DMF. To the swollen resin 250 ml of 20% piperidine in DMF is added and stirred for 20 min. The reactor is emptied through the filter in the bottom by applying vacuum to the reactor and a second treatment with 250 ml 20% piperidine in DMF is performed for 20 min. The reactor is once again emptied by applying vacuum to it followed by a wash of the peptide resin using 2 L of DMF. The reactor is then emptied by applying vacuum. The peptide resin is now ready for step 2.
Step 2. A solution of 27.0 g Fmoc-D-Ala-OH (2 eq.), 14.3 g HOBt and 13.2 ml DIC is dissolved in 250 ml of DMF and allowed to activate for 15 min, after which it is poured into the reactor containing the peptide resin. After 1 h of reaction time, 2.2 ml of NMM is added to the solution and the reaction is allowed to proceed for another hour. Then 30 ml acetic acid anhydride and 2 ml NMM is added to the mixture, which is allowed to stand under stirring for 15 min. Then the reactor is emptied by using vacuum. The peptide resin is washed with 2 L DMF. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 250 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second treatment of 250 ml 20% piperidine in DMF for 20 min is performed. The reactor is once again emptied by applying vacuum and the peptide resin is washed with 2 L of DMF. It is now ready for step 3.
Step 3. A solution of 29 g Fmoc-L-Pro-OH (2 eq), 14.3 g HOBt and 13.2 ml DIC is dissolved in 250 ml DMF and allowed to activate for 25 min, after which it is poured into the reactor containing the peptide resin. After 75 min of reaction, 2.2 ml NMM is added to the solution, and the reaction is allowed to proceed for another hour. Then 30 ml acetic acid anhydride and 2 ml NMM is added to the mixture, which is allowed to stand under stirring for 15 min, The reactor is then emptied by using vacuum. DMF (2.6 L) is used for washing the peptide resin. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 250 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum, and a second treatment with 250 ml 20% piperidine in DMF for 20 min is performed. The reactor is once again emptied by applying vacuum and the peptide resin is washed with 2 L of DMF. It is now ready for step 4.
Step 4. A solution of 33 g Fmoc-L-ILys(Boc)-OH (1.5 eq), 10.7 g HOBt and 10.1 ml DIC is dissolved in 250 ml of DMF and allowed to activate for 0.5 h, after which it is poured into the reactor containing the peptide resin. After 2 h of reaction, 2.2 ml NMM is added to the solution and the reaction is allowed to proceed for another hour. Then 30 ml acetic acid anhydride and 2.2 ml NMM is added to the mixture, which is allowed to stand under stirring for 15 min, whereupon the reactor is emptied by using vacuum. The peptide resin is washed with DMF (3 L). After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 250 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second treatment of 250 ml 20% piperidine in DMF for 20 min is performed. The reactor is once again emptied by applying vacuum and the peptide resin is washed with 3.5 L DMF. It is now ready for step 5.
Step 5. A solution of 38 g Fmoc-L-Leu-OH (2.5 eq), 18 g of HOBt and 16.8 ml of DIC is dissolved in 250 ml of DMF and allowed to activate for 0.5 h, after which it is poured into the reactor containing the peptide resin. After 2 h of reaction, 2.2 ml NMM is added to the solution, and the reaction is allowed to proceed for another 50 min. Then 30 ml acetic acid anhydride and 2 ml NMM is added to the mixture, which is allowed to stand under stirring for 15 min. Then the reactor is emptied by using vacuum. DMF (2.6 L) is used for washing the peptide resin. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 250 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second treatment with 250 ml 20% piperidine in DMF for 20 min is performed. The reactor is once again emptied by applying vacuum and the peptide resin is washed with 2.5 L of DMF. It is now ready for step 6.
Step 6. A solution of 32 g of Fmoc-D-4Aph(tBu-Cbm)-OH (1.5 eq), 10.7 g HOBt and 10.1 ml DIC is dissolved in 250 ml of DMF and allowed to activate for 1 hour, after which it is poured into the reactor containing the peptide resin. After 20 min of reaction, 22 ml NMM is added to the solution and the reaction is allowed to proceed for another 20 h. Then 30 ml acetic acid anhydride and 2 ml NMM is added to the mixture, which is allowed to stand under stirring for 15 min. Then the reactor is emptied by using vacuum. The peptide resin is washed with 4 L DMF. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 250 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second 20 min treatment with 250 ml 20% piperidine in DMF is performed. The reactor is once again emptied by applying vacuum and the peptide resin is washed with 3.4 L DMF. It is now ready for step 7.
Step 7. A solution of 35 g Fmoc-L-4Aph(L-Hor)-OH (1.5 eq), 11 g HOBt and 10.1 ml DIC is dissolved in 350 ml DMF and allowed to activate for 1 h, after which it is poured into the reactor containing the peptide resin. After 50 min of reaction, 2.2 ml NMM is added to the solution and the reaction is allowed to proceed for another 21.5 h. The reactor is emptied by using vacuum. The peptide resin is washed with 4.4 L DMF. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 350 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second 20 min treatment with 350 ml 20% piperidine in DMF is performed. The reactor is once again emptied by applying vacuum and the peptide resin is washed with 4.4 L DMF. It is now ready for step 8.
Step 8. Fmoc-L-Ser(tBu)-OH (2.5 eq) (41 g), 17.9 g HOBt, 16.8 ml DIC and 4.9 ml of NMM is dissolved in 500 ml of DMF and poured into the reactor containing the peptide resin. The reaction is allowed to proceed for 3.5 h. The reactor is then emptied by using vacuum. The peptide resin is washed with 4.2 L DMF. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 375 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second 20 min treatment of 375 ml 20% piperidine in DMF is performed. The reactor is once again emptied by applying vacuum and the peptide resin washed with 4.2 L of DMF. It is now ready for step 9.
Step 9. A solution of 25 g Fmoc-D-3 Pal-OH (1.5 eq), 10.7 g HOBt, 10.1 ml DIC and 4.9 ml NMM is dissolved in 400 ml of DMF and poured into the reactor containing the peptide resin. The reaction is allowed to proceed for 4.5 h. Then the reactor is emptied by using vacuum. The peptide resin is washed with 4.2 L DMF. After applying vacuum to the reactor, removing the DMF, the peptide resin is treated with 375 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second 20 min treatment with 375 ml 20% piperidine in DMF is performed. The reactor is once again emptied by applying vacuum and the peptide resin washed with 4.2 L of DMF. It is now ready for step 10.
Step 10. A solution of 27 g Fmoc-D-Phe(4Cl)—OH (1.5 eq), 10.7 g HOBt, 10.1 ml DIC and 4.9 ml NMM is dissolved in 400 ml of DMF and is poured into the reactor containing the peptide resin. The reaction is allowed to proceed for 10 h. The reactor is emptied by using vacuum. The resin is washed with 5.5 L DMF. After applying vacuum to the reactor and removing the DMF, the peptide resin is treated with 375 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second 20 min treatment with 375 ml 20% piperidine in DMF is performed. The reactor is once again emptied by applying vacuum and the peptide resin washed with 5 L DMF. It is now ready for step 11.
Step 11. A solution of 28 g Fmoc-D-2Nal-OH (1.5 eq), 10.7 g HOBt, 10.1 ml DIC and 4.9 ml NMM is dissolved in 400 ml DMF and poured into the reactor containing the peptide resin. The reaction is allowed to proceed for 2.5 h. The reactor is emptied by using vacuum. The peptide resin is washed with 5.2 L DMF. After applying vacuum to the reactor and removing the DMF, the peptide resin is treated with 375 ml of 20% piperidine in DMF for 20 min. The reactor is emptied by applying vacuum and a second 20 min treatment of 375 ml 20% piperidine in DMF is performed. The reactor is once again emptied by applying vacuum and the peptide resin washed with 5 L DMF. It is now ready for and is ready for step 12.
Step 12. Acetylimidazole (3 eq) (14.5 g) and 4.9 ml NMM is dissolved in 400 ml DMF and poured into the reactor. After 1.5 h, the reactor is emptied by applying vacuum to the reactor. The peptide resin is washed with 5 L DMF and the reactor emptied using vacuum.
Step 13. The peptide resin is washed with WA and dried under vacuum. Peptide resin (129.8 g; yield 96%) was isolated.
Step 14. Dry peptide resin (60 g) is suspended in 600 ml TFA for 25 h at room temperature. It was then poured into a mixture of 2.4 L water, 620 g ammonium acetate, 600 ml ethanol and 600 ml acetic acid. The mixture is adjusted to a pH between 3 and 4 using TFA and filtered.
Step 15. The product is purified using a two step purification protocol. In the first step a column (2.5 cm×34 cm) packed with reversed phase C-18 material is used with a buffer system consisting of buffer A (0.12% aqueous TFA) and buffer B (99.9% ethanol) A volume from the filtered solution from step 14 corresponding to 1.6 g of the product is applied to the column. Purification is executed using a step gradient starting with 10% B for 2-3 column volumes, 29% B for 5-7 column volumes and a gradient from 29% B to 50% B over 3 column volumes at a flow rate of 70 ml/min. This procedure is followed until all the filtered solution from step 14 has been processed. All fractions collected are analyzed by analytical HPLC. Fractions containing product with a purity higher than 94% are pooled. The second purification step is performed using a column (2.5 cm×34 cm) packed with reverse phase C-18 material and a buffer system consisting of a buffer A (1% aqueous acetic acid), buffer B (99.9% ethanol), and buffer C (0.5 M aqueous ammonium acetate). From the pooled fractions containing the product an amount equivalent to 1.3 g of the product is applied to the column and purification performed by applying a step gradient starting with 10% B+90% C for 2-3 column volumes followed by 90% A+10% B for 2-3 column volumes. The product is eluted by 24% B+76% A. The fractions containing product with the acceptable purity are pooled and desalted using the same column. Desalting is performed using buffer A (1% aqueous acetic acid) and buffer B (99.9% ethanol). A volume from the pooled purified fraction corresponding to 1.6 g of product is applied to the column, 2-3 column volumes buffer A being used to wash out any ammonium acetate in the product. Then the product is eluted using 50% buffer A+50% buffer B. The solution of the purified product containing 50% ethanol is concentrated on a rotary evaporator. When all the ethanol has been removed the remaining solution containing the product is lyophilized. A total of 11.8 g (overall yield 37%) of degarelix is obtained as a fluffy solid. 4-([2-(5-Hydantoyl)]acetylamino)-phenylalanine could not be detected in the product (HPLC).
Example 4 Synthesis and Purification of Degarelix Using Fmoc-Rink Amide MBHA
Performed substantially as the synthesis and purification of Example 1. Deviations from the method of Example 1:
4-([2-(5-Hydantoyl)]acetylamino)-phenylalanine could not be detected in the product by HPLC.
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http://www.google.com/patents/EP2447276A1?cl=en
where Ac is acetyl, 2Nal is 2-naphthylalanine, 4Cpa is 4-chlorophenylalanine, 3Pal is 3-pyridylalanine, Ser is serine, 4Aph is 4-aminophenylalanine, Hor is hydroorotyl, Cbm is carbamoyl, Leu is leucine, Lys(iPr) is N6-isopropyllysine, Pro is proline and Ala is alanine.
Starting materials:
| N-t-Butyloxycarbonyl-D-4-chlorophenylalanine | Boc-D-4Cpa-OH C14H18NO4 |
| N-t-Butyloxycarbonyl-D-2-naphtylalanine | Boc-D-2Nal-OH C18H21N04 |
| D-3-Pyridylalanine hydrochloride | H-D-3Pal-OH x 2HCl C8H12Cl2N2O2 |
| N-α-t-Butyloxycarbonyl-N-4-(t-Butylcarbamoyl)-D-4-Aminophenylalanine | Boc-D-4Aph(tBuCbm)-OH C19H29N3O5 |
| N-α-t-Butyloxycarbonyl-N-4-(L-Hydroorotyl)-4-Aminophenylalanine | Boc-4Aph(L-Hor)-OH C19H24N4O7 |
| Leucine benzyl ester p-tosylate | H-Leu-OBzl x TOS C20H27NO5 |
| N-Benzyloxycarbonyl-O-t-butyl-serine | Z-Ser(tBu)-OH C8H15NO5 |
| N-t-Butyloxycarbonyl-proline | Boc-Pro-OH C10H17NO4 |
| D-Alaninamide hydrochloride | H-D-Ala-NH2 x HCl C3H8ClNO2 |
| N-α-Benzyloxycarbonyl-N-ε-t-butyloxycarbonyl-N-ε-isopropyl-lysine, dicyclohexylamine salt | Z-Lys(iPr,Boc)-OH x DCHA C34H57N3O6 |
Example 1: Synthesis of Intermediate Ac(1-3)ONa: Ac-D-2Nal-D-4Cpa-D-3Pal-ONa[7]Activation of Boc-D-4Cpa-OH and isolationStep 1 (Reaction step)
Activation of Boc-D-2Nal-OH and isolationStep 2 (reaction step)
Synthesis of Boc(2-3)OH: Boc-D-4Cpa-D-3Pal-OHStep 3 (Reaction step)
Synthesis of Intermediate Ac(1-3)ONa: Ac-D-2Nal-D-4Cpa-D-3Pal-ONa[7] (Compound of formula IIIa)Step 4 (Reaction step)
Example 2: Synthesis of Intermediate Z(4-7)OH x DCHA: Z-Ser(tBu)-4Aph(L-Hor)-D-4Aph(tBuCbm)-Leu-OHxDCHA[15]Synthesis of intermediate Boc(6-7)OBzl: Boc-D-4Aph(tBucbm)-Leu-OBzl Step 5 (Reaction step)
Synthesis of Boc-(5-7)-OBzl: Boc-4Aph(L-Hor)-D-4Aph(tBucbm)-Leu-OBzlStep 6 (Reaction step)
Synthesis of intermediate Z(4-7)OH x DCHA: Z-Ser(tBu)-4Aph(L-Hor)-D-4Aph(tBuCbm)-Leu-OH x DCHA (Compound of formula Va)Step 7 (Reaction step)
Example 3: Synthesis of Intermediate H(8-10)NH 2 :H-Lys(iPr,Boc)-Pro-D-Ala-NH 2 [21]Synthesis of Boc(9-10)NH2: Boc-Pro-D-Ala-NH2Step 8 (Reaction step)
Synthesis of intermediate H(8-10)NH2: H-Lys(iPr,Boc)-Pro-D-Ala-NH2 (Compound of formulae Vla)Step 9 (Reaction step)
Example 4: Segment Condensations to Final Intermediate (compound of Formula II)intermediate Z(4-10)NH2 : Z-Ser(tBu)-4Aph(L-Hor)-D-4Aph(tBuCbm)-leu-lys(iPr,Boc)-Pro-D-Ala-NH2[22]
Step 10 (reaction step)
Final Intermediate Ac(1-10)NH2: Ac-D-2Nal-D-4Cpa-D-3Pal-Ser(tBu)-4Aph(L-Hor)-D-4Aph(tBuCbm)-leu-Lys(iPr, Boc)-Pro-D-Ala-NH2[24]Step 11 (Reaction step)
Example 5: Deprotection of Final Intermediate Ac(1-10)NH 2 to Crude Degarelix[251]Step 12 (Reaction step)
Step 13 (purification and lyophilisation)












…………….
After conversion to the corresponding urea by treatment with tert-butyl isocyanate, the Boc group was cleaved with TFA to produce resin (XIII). Further coupling with N-alpha- Boc-L-4-(Fmoc-amino)phenylalanine (XIV), followed by Fmoc deprotection with piperidine, furnished (XV). The aniline derivative (XV) was acylated with L-hydroorotic acid (XVI) to yield, after Boc group cleavage, resin (XVII). Coupling of (XVII) with N- Boc-L-serine(O-benzyl) (XVIII) and subsequent deprotection gave (XIX), as shown in Scheme 2, below:
Peptide (XIX) was sequentially coupled with N-alpha-Boc-D-(3-pyridyl)alanine (XX) and N-Boc-D-(4-chlorophenyl)alanine (XXII) to furnish, after the corresponding deprotection cycles with TFA, the resins (XXI) and (XXIII), respectively, as shown in Scheme 3, below:
The coupling of resin (XXIII) with N-Boc-D-(2-naphthyl)alanine (XXIV) as before gave, after the corresponding deprotection cycle with TFA, resin (XXV). The peptide resin (XXV) was acetylated with Ac20 and finally deprotected and cleaved from the resin by treatment with HF to provide the target peptide, as shown in Scheme 4 below:
Alternatively, after coupling of the peptide resin (XIII) with alpha-Boc-L-4-(Fmoc- amino)-phenylalanine (XIV), the Fmoc protecting group was not removed, yielding resin (XXVI). Subsequent coupling cycles with amino acids (XVIII), (XX), (XXII) and (XXIV) as above finally produced resin (XXVII). The Fmoc group was then deprotected by treatment with piperidine, and the resulting aniline was acylated with L-hydroorotic acid (XVI) to provide resin (XXVIII), as shown in Scheme 5 below:
Resin (XXVIII) was finally cleaved and deprotected by treatment with HF, as shown in Scheme 6 below:
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Nigella Sativa Kills 89% of Lung Cancer Cells in Vitro: Researchers have just shown that nigella sativa (also known as black seed or black cumin) seed oil killsup to 89% of human lung cancer cells (A-549) after just 24 hours, while a non-oil extract from the seeds killed up to 77% of the cancer cells.
The extracts were prepared from seeds obtained at a local market. Nigella sativa is a powerful medicinal herb which has been used for thousands of years in traditional Chinese, Ayurvedic, Unani and Arabic medicine. It is best known for its potent anti-inflammatory and antioxidant properties, and has been used to suppress coughs, treat kidney stones, diarrhea and stomach pain. But modern science has now also uncovered nigella’s powerful anti-diabetes and anti-cancer effects.
This super herb has already shown potent activity against cancer of the breast, prostate, kidney, pancreas, liver, colon and cervix in previous lab studies, and this new study has shown new activity against lung cancer. Good health and cancer prevention should always start with a well-balanced diet focused on organic vegetables, fruit and whole foods (consuming at least half in the raw state). But nigella sativa may offer sizeable benefits for those wanting an extra measure of protection.
read at
http://www.ncbi.nlm.nih.gov/pubmed/24568529
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Nigella sativa is an annual flowering plant, native to south and southwest Asia. It grows to 20–30 cm (7.9–11.8 in) tall, with finely divided, linear (but not thread-like) leaves. The flowers are delicate, and usually coloured pale blue and white, with five to ten petals. The fruit is a large and inflated capsule composed of three to seven united follicles, each containing numerous seeds. The seed is used as a spice.
The scientific name is a derivative of Latin niger (black).[2]
In English, Nigella sativa seed is variously called fennel flower,[3] nutmeg flower,[3] black caraway,[3] Roman coriander,[3] and also called black cumin.[3] Other names used, sometimes misleadingly, are onion seed and black sesame, both of which are similar-looking, but unrelated.Blackseed and black caraway may also refer to Bunium persicum.[4]
The seeds are frequently referred to as black cumin (as in Assamese: kaljeera or kolajeera or Bengali kalo jeeray), But black cumin (kala Jeera)[clarification needed] is different than Nigella sativa (Kali Jeeri).[citation needed] In south Indian language Kannada it is called [ಕೃಷ್ಣ ಜೀರಿಗೆ] “Krishna Jeerige”, but this is also used for a different spice, Bunium persicum.
In English-speaking countries with large immigrant populations, it is also variously known as kaljeera (Assamese কালজীৰা kalzira or ক’লাজীৰাkolazira), kalo jira (Bengali: কালোজিরা kalojira, black cumin), karum cheerakam, habbat al-barakah (Arabic حبة البركة) Kurdish “reşke” (rashkeh) (Tamil கருஞ்சீரகம்), kalonji (Hindi कलौंजी kalauṃjī or कलोंजी kaloṃjī, Urdu كلونجى kaloṃjī) or mangrail (Hindi मंगरैल maṃgarail), “Kala Jira in Marathi” ketzakh (Hebrew קצח), chernushka (Russian), çörek otu (Turkish), garacocco (Cypriot Turkish), ḥebbit al-barakah, seed of blessing (Arabic), siyah daneh (Persian سیاهدانه siyâh dâne), jintan hitam (Indonesian), karim jeerakam (കരിംജീരകം) in Malayalamor කළු දුරු in Sinhala, Karto Jeera in Beary.
It is used as part of the spice mixture paanch phoran or panch phoron (meaning a mixture of five spices) and by itself in a great many recipes in Bengali cookery and most recognizably in naan bread.[5]
The Turkish name çörek otu literally means “bun’s herb” from its use in flavouring the çörek buns. Such braided-dough buns are widespread in the cuisines of Turkey and its neighbours (see Tsoureki τσουρέκι). In Bosnian, the Turkish name for Nigella sativa is respelled as čurekot. The seed is used in Bosnia, and particularly its capital Sarajevo, to flavour pastries (Bosnian: somun) often baked on Muslim religious holidays.
The Arabic approbation about Bunium bulbocastanum (Kaala Jeera) Hebbit il barakah, meaning the “seed of blessing” is also applied toNigella sativa (Kali Jeeri).
Nigella sativa has a pungent bitter taste and smell. It is used primarily in confectionery and liquors. Peshawari naan is, as a rule, topped with kalonji seeds. Nigella is also used in Armenian string cheese, a braided string cheese called Majdouleh or Majdouli in the Middle East.
According to Zohary and Hopf, archaeological evidence about the earliest cultivation of N. sativa “is still scanty”, but they report supposed N. sativa seeds have been found in several sites from ancient Egypt, including Tutankhamun‘s tomb.[6] Although its exact role in Egyptian culture is unknown, it is known that items entombed with a pharaoh were carefully selected to assist him in the afterlife.
The earliest written reference to N. sativa is thought to be in the book of Isaiah in the Old Testament, where the reaping of nigella and wheat is contrasted (Isaiah 28: 25, 27). Easton’s Bible dictionary states the Hebrew word ketsah refers to N. sativa without doubt (although not all translations are in agreement). According to Zohary and Hopf, N. sativawas another traditional condiment of the Old World during classical times; and its black seeds were extensively used to flavour food.[6]
Found in Hittite flask in Turkey from 2nd millennium BCE.[7]

The black cumin (Bunium bulbocastanum) seeds have been traditionally used in the Middle East and Southeast Asian countries for a variety of ailments. Nigella seeds are sold as black cumin in small bundles to be rubbed until warm, when they emit an aroma similar to black cumin which opens clogged sinuses in the way that do eucalyptus or Vicks.
Nestlé has purportedly filed a patent application covering use of Nigella sativa as a food allergy treatment.[10] Yet the firm denies the claim of patenting the plant, stating that the patent would only cover “the specific way that thymoquinone – a compound that can be extracted from the seed of the fennel flower – interacts with opioid receptors in the body and helps to reduce allergic reactions to food”.[11]
Thymoquinone, found in the seed oil extract of N. sativa, has been shown to have anti-neoplastic effects in rats and mice and in cultured human cells from several types of cancer, including pancreatic ductal adenocarcinoma.[12] It has protective antioxidant and anti-inflammatory effects, and promotes apoptosis (cell death) of the cancer cells.[12]
Original black cumin (Bunium bulbocastanum) is rarely available, so N. sativa is widely used instead; in India, Carum carvi is the substitute. Cumins are from the Apiaceae (Umbelliferae) family, but N. sativa is from Ranunculaceae family. Black cumin (not N. sativa) seeds come as paired or separate carpels, and are 3–4 mm long. They have a striped pattern of nine ridges and oil canals, and are fragrant (Ayurveda says, “Kaala jaaji sugandhaa cha” (black cumin seed is fragrant itself)), blackish in colour, boat-shaped, and tapering at each extremity, with tiny stalks attached; it has been used for medicinal purposes for centuries, both as a herb and pressed into oil, in Asia, the Middle East, and Africa.
Nigella sativa oil contains an abundance of conjugated linoleic (18:2) acid, thymoquinone, nigellone (dithymoquinone),[13] melanthin, nigilline,damascenine, and tannins. Melanthin is toxic in large doses and nigelline is paralytic, so this spice must be used in moderation.


Cuban doctors have filed Wednesday in Havana, the result of 14 years of research, a solution of antitumor peptides whose natural analogue is able to offer positive dynamics in cancer treatments
http://youthandeldersja.wordpress.com/2014/03/22/cuba-may-have-found-cure-for-cancer/
burdock
dandelionDandelion root and burdock root are my two most commonly prescribed herbs when chronic conditions require anti-inflammatory, blood purifying alteratives for gentle detoxification. This includes conditions such as arthritis and cancer. I’ve studied literally hundreds of herbs from around the world, and considering cost, availability, palatability (no small matter, as people with chronic disease like cancer need to be able to take their herbs at least three times a day for months) – there are probably no two more simple and powerful anticancer herbs on the planet than dandelion and burdock.*
After prescribing both of these in strong dose clinically for years with great results (patients feel better, or experience slowing or even complete remission of some cancers), I learned that many professional British medical herbalists also use the same two-herb combination for conditions requiring blood, lymphatic and liver detoxification.
http://www.planetherbs.com/michaels-blog/dandelion-burdock-and-cancer.html
Moringa Oleifera Kills 97% of Pancreatic Cancer Cells in Vitro:

A hot-water extract of moringa leaves was shown to kill up to 97% of human pancreatic cancer cells (Panc-1) after 72 hours in this study. Moringa, also called the “miracle tree,” has a long history of use in traditional and Ayurvedic medicine due to its many beneficial properties as an anti-fungal, anti-bacterial, antidepressant, anti-diabetes, pain and fever reducer and even relief from asthma. But it also contains numerous powerful anti-cancer compounds such as kaempferol, rhamnetin, isoquercetin and others.
Latest research is now proving out moringa’s anti-cancer potential with positive results so far against ovarian cancer, liver cancer, lung cancer, and melanoma. Moringa is now extensively cultivated throughout Southeast Asia, Oceania, the Caribbean and Central America, but the largest crop in the world is produced by India – where it grows natively.
That may be one reason why the death rate from pancreatic cancer in India is a stunning 84% lower than in the United States.
http://www.ncbi.nlm.nih.gov/pubmed/23957955

