Seldegamadlin

 

Seldegamadlin

CAS 2713618-08-5

MFC48H52Cl2FN7O6 MW912.9 g/mol

• (3'R,4'S,5'R)-6''-chloro-4'-(3-chloro-2-fluorophenyl)-N-((1r,4R)-4-(4-(1-(2,6-dioxopiperidin-3-yl)-3-methyl-2-oxo-2,3-dihydro-1H-benzo[d]imidazol-5-yl)piperidine-1-carbonyl)cyclohexyl)-2''-oxodispiro[cyclohexane-1,2'-pyrrolidine-3',3''-indoline]-5'-carboxamide
• (3'R,4'S,5'R)-6"-chloro-4'-(3-chloro-2-fluorophenyl)-N-((1r,4R)-4-(4-(1-(2,6-dioxopiperidin-3-yl)-3-methyl-2-oxo-2,3-dihydro-1H-benzo[d]imidazol-5-yl)piperidine-1-carbonyl)cyclohexyl)-2''-oxodispiro[cyclohexane-1,2'-pyrrolidine-3',3"-indoline]-5'-carboxamide

(3'R,4'S,5'R)-6''-chloro-4'-(3-chloro-2-fluorophenyl)-N-[trans-4-(4-{1-[(3RS)-2,6-dioxopiperidin-3-yl]-3-methyl-2-oxo-2,3-dihydro-1H-1,3-benzimidazol-5-yl}piperidine-1-carbonyl)cyclohexyl]-2''-oxo-1'',2''-dihydrodispiro[cyclohexane-1,2'-pyrrolidine-3',3''-indole]-5'-carboxamide
E3 ubiquitin-protein ligase Mdm2 (Hdm2) degrader, antineoplastic, KT 253, KT-253, VNP2BV6KGL

Seldegamadlin (also known as KT-253) is an advanced experimental oncology drug designed as a first-in-class, highly potent MDM2 PROTAC degrader and p53 stabilizer. It utilizes targeted protein degradation (TPD) technology to selectively eliminate the MDM2 oncoprotein, which restores the normal function of the critical tumor suppressor protein, p53.

How it Works

• Targeted Protein Degradation: It acts as a heterobifunctional PROTAC (proteolysis-targeting chimera). It features one end that binds tightly to MDM2 and another end that recruits the cereblon (CRBN) E3 ubiquitin ligase.
• p53 Stabilization: By tethering them together, it forces the cell's natural disposal machinery to ubiquitinate and rapidly destroy MDM2. Because MDM2 normally suppresses and destroys p53, deleting MDM2 leads to an immediate up-regulation and stabilization of active p53.
• Apoptosis Activation: The sudden resurgence of active p53 fires up downstream targets like p21, forcing wild-type p53 cancer cells to halt their cell cycle (at the G2/M phase) and trigger rapid programmed cell death (apoptosis).

Primary Areas of Research

Seldegamadlin is actively being evaluated and researched for therapeutic efficacy against specific wild-type p53 malignancies:

• Hematologic Tumours: Including Acute Myeloid Leukemia (AML) and Acute Lymphoblastic Leukemia (ALL).
• Solid Tumours: Such as Diffuse Large B-cell Lymphoma (DLBCL) and other forms retaining functional p53 signaling pathways

PAT

WO2023049790

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2023049790&_cid=P11-MTWC17-46822-1

[001997] 3-[5-[1-(4-aminocyclohexanecarbonyl)-4-piperidyl]-3-methyl-2-oxo-benzimidazol-1-

yl]piperidine-2,6-dione (Intermediate WP)

[001998] Step 1 - Tert-butyl N-[4-[4-[1-(2,6-dioxo-3-piperidyl)-3-methyl-2-oxo-benzimidazol-5-yl]piperidine-1-carbonyl]cyclohexyl]carbamate. A mixture of 3-[3-methyl-2-oxo-5-(4-piperidyl)benzimidazol-1-yl]piperidine-2,6-dione (200 mg, 584 umol, Intermediate HE), (1s,4s)-4-((tert-butoxycarbonyl)amino)cyclohexane-1-carboxylic acid (142 mg, 584 umol, CAS# 53292-90-3), 1-methylimidazole (1.53 g, 18.6 mmol) , and TCFH (409 mg, 1.46 mmol) in ACN (1 mL) was stirred at 25 °C for 1 min. On completion, the reaction mixture was concentrated to give a residue. The crude product was purified by reversed-phase HPLC (0.1% FA condition) to give the title compound (120 mg, 36% yield) as a white solid.1H NMR (400 MHz, DMSO-d6) δ 11.08 (s, 1H), 7.11 (s, 1H), 7.02 (d, J = 8.0 Hz, 1H), 6.92 (d, J = 8.0 Hz, 1H), 5.34 (dd, J = 5.6, 12.8 Hz, 1H), 4.62 - 4.54 (m, 1H), 4.10 - 3.98 (m, 1H), 3.49 ( s, 1H), 3.33 - 3.31 (m, 4H), 3.18 - 3.05 (m, 1H), 2.96 - 2.85 (m, 1H), 2.83 - 2.74 (m, 1H), 2.71 -2.62 (m, 3H), 2.05 - 1.94 (m, 1H), 1.86 - 1.67 (m, 6H), 1.61 - 1.40 (m, 7H), 1.39 (s, 9H).

[001999] Step 2 - 3-[5-[1-(4-aminocyclohexanecarbonyl)-4-piperidyl]-3-methyl-2-oxo-benzimidazol -1-yl]piperidine-2,6-dione. To a solution of tert-butyl N-[4-[4-[1-(2,6-dioxo-3-piperidyl)-3-methyl-2-oxo-benzimidazol-5-yl] piperidine-1-carbonyl]cyclohexyl]carbamate (60.0 mg, 105 umol) in DCM (1 mL) was added TFA (1.54 g, 13.5 mmol). The mixture was then stirred at 25 °C for 2 mins. On completion, the mixture was concentrated in vacuo to give the title compound (50.0 mg, 80% yield, TFA) as brown oil. LC-MS (ESI+) m/z 468.1 (M+H)⁺.

[00812] (3'R,4'S,5'R)-6''-chloro-4'-(3-chloro-2-fluorophenyl)-2''-oxodispiro[cyclohexane-1,2'-pyrrolidine-3',3''-indoline]-5'-carboxylic acid (Intermediate CI)

[00813] Step 1 - (3E)-6-chloro-3-[(3-chloro-2-fluoro-phenyl)methylene]indolin-2-one. A 500 mL 3-necked round bottom flask was charged with 6-chloroindolin-2-one (89.6 g, 535 mmol, CAS# 56341-37-8), 3-chloro-2-fluoro-benzaldehyde (84.8 g, 535 mmol, CAS# 85070-48-0), MeOH (1700 mL) and piperidine (9.11 g, 107 mmol). The mixture was stirred at 65 °C for 5 h, then at 25 °C for 12 h. On completion, the reaction mixture was filtered and the filter cake was dried under reduced pressure to give title product (160 g, 94% yield).¹H NMR (400 MHz, DMSO-d6) δ = 10.87 (s, 1H), 7.82 - 7.63 (m, 2H), 7.56 (s, 1H), 7.39 (t, J = 8.0 Hz, 1H), 7.18 (d, J = 8.0 Hz, 1H), 7.03 - 6.77 (m, 2H).

[00814] Step 2 - (E)-6-chloro-3-(3-chloro-2-fluorobenzylidene)indolin-2-one. (3E)-6-chloro-3-[(3-chloro-2-fluoro-phenyl)methylene]indolin-2-one (50 g, 162 mmol), (5R,6S)-5,6-diphenylmorpholin-2-one (49.3 g, 194 mmol, CAS# 282735-66-4), and cyclohexanone (31.8 g, 324 mmol, 33.6 mL) were dissolved in THF (75 mL) and toluene (750 mL) and 140 ºC for 12 hours. On completion, the reaction mixture was concentrated in vacuo to give a residue. The residue was purified by column chromatography (SiO2, petroleum ether/ethyl acetate=8/1 to 5/1) to give the title compound (160 g 97% purity).¹H NMR (400 MHz, DMSO-d₆) δ = 10.79 (s, 1H), 7.95 ( t, J = 6.8 Hz, 1H), 7.45 - 7.37 (m, 1H), 7.33 - 7.20 (m, 4H), 7.18 - 7.09 (m, 4H), 7.07 - 6.98 (m, 2H), 6.86 - 6.75 (m, 3H), 6.66 (dd, J = 2.0, 8.4 Hz, 1H), 6.35 (d, J = 8.4 Hz, 1H), 5.44 (d, J = 11.2 Hz, 1H), 4.90 (d, J = 2.8 Hz, 1H), 4.58 (d, J = 11.2 Hz, 1H), 2.39 (d, J = 12.8 Hz, 1H), 2.24 - 2.09 (m, 1H), 1.42 - 1.18 (m, 4H), 1.10 - 0.78 (m, 1H).

[00815] Step 3 - (3'S,4'R,7'R,8'S,8a'R)-6''-chloro-8'-(3-chloro-2-fluorophenyl)-3',4'-diphenyl-3',4',8',8a'-tetrahydro-1'H-dispiro[cyclohexane-1,6'-pyrrolo[2,1-c][1,4]oxazine-7',3''-indoline]-1',2''-dione. H₂SO₄ (9.07 g, 92.5 mmol, 4.93 mL) was added to a solution of intermediate (E)-6-chloro-3-(3-chloro-2-fluorobenzylidene)indolin-2-one (9.0 g, 14.03 mmol) dissolved in MeOH (70 mL) and the resulting solution was heated to 50 °C for 5 hours. On completion, the reaction mixture was cooled to 0 °C and slowly neutralized with a solution of saturated sodium bicarbonate. The aqueous solution was extracted with ethyl acetate, and the organic layer was dried over sodium sulfate, filtered, concentrated to give the residue. The residue was purified by reverse phase flash [ACN/(0.1% FA in water), 0% to 90% ] to give title compound (7.0 g 84.2% purity).¹H NMR (400 MHz, DMSO-d6) δ = 7.74 - 7.68 (m, 1H), 7.57 (s, 1H), 7.51 (d, J = 8.4 Hz, 1H), 7.41 (d, J = 7.2 Hz, 4H), 7.25 (d, J = 7.6 Hz, 6H), 7.19 - 7.11 (m, 6H), 7.10 - 6.98 (m, 4H), 6.94 - 6.88 (m, 1H), 6.65 - 6.58 (m, 1H), 5.39 - 5.27 (m, 1H), 4.89 - 4.75 (m, 1H), 4.42 -4.29 (m, 2H), 4.04 (q, J = 6.8 Hz, 1H), 3.63 - 3.53 (m, 2H), 3.40 (s, 3H), 2.22 - 2.12 (m, 1H), 2.05 - 1.94 (m, 3H), 1.40 - 1.32 (m, 2H), 1.28 - 1.13 (m, 3H).

[00816] Step 4 - Methyl (3'R,4'S,5'R)-6''-chloro-4'-(3-chloro-2-fluorophenyl)-1'-((1R,2S)-2-hydroxy-1,2-diphenylethyl)-2''-oxodispiro[cyclohexane-1,2'-pyrrolidine-3',3''-indoline]-5'-carboxylate. The resulting intermediate (3'S,4'R,7'R,8'S,8a'R)-6''-chloro-8'-(3-chloro-2-fluorophenyl)-3',4'-diphenyl-3',4',8',8a'-tetrahydro-1'H-dispiro[cyclohexane-1,6'-pyrrolo[2,1-c][1,4]oxazine-7',3''-indoline]-1',2''-dione (7.0 g, 10.3 mmol) was dissolved in ACN (78 mL), then CAN (11.3 g, 20.7 mmol) was added, followed by the addition of H2O (78 mL). The reaction was stirred at 25 °C for 30 min. On completion, the reaction mixture was quenched by adding the mixture to a cold saturated aqueous NaHCO3 solution (50 mL). The aqueous layer was extracted with ethyl acetate (20 mL x 3). The organic layer was separated, dried over anhydrous Na2SO4, filtered and concentrated under reduced pressure to give the residue. The residue was purified by column chromatography (SiO2, petroleum ether/ethyl acetate=50/1 to 5/1) to give title compound (1.58 g, 31% purity). LC-MS (ESI⁺) m/z 477.2 (M+H)⁺.

[00817] Step 5 - (3'R,4'S,5'R)-6''-chloro-4'-(3-chloro-2-fluorophenyl)-2''-oxodispiro[cyclohexane-1,2'-pyrrolidine-3',3''-indoline]-5'-carboxylic acid. Methyl (3'R,4'S,5'R)-6''-chloro-4'-(3-chloro-2-fluorophenyl)-1'-((1R,2S)-2-hydroxy-1,2-diphenylethyl)-2''-oxodispiro[cyclohexane-1,2'-pyrrolidine-3',3''-indoline]-5'-carboxylate (2.00 g, 4.19 mmol) was dissolved in THF (14 mL) and LiOH^.H₂O (527 mg, 12.5 mmol) was added followed by water (14 mL) and MeOH (2 mL) and the reaction was stirred at 25 °C for 15 min. On completion, water (20 mL) was added and the reaction was slowly neutralized with 2M HCl and the suspension was stirred for 15 min. The resulting precipitate was filtered, washed with water to give title compound (1.50 g, 70% yield).¹H NMR (400 MHz, DMSO-d₆) δ = 10.75 - 10.57 (m, 1H), 10.55 (s, 1H), 7.61 - 7.54 (m, 1H), 7.50 - 7.44 (m, 1H), 7.41 - 7.34 (m, 1H), 7.18 - 7.12 (m, 1H),

7.08 - 7.02 (m, 1H), 6.72 - 6.66 (m, 1H), 4.72 - 4.65 (m, 1H), 4.54 - 4.47 (m, 1H), 3.18 - 3.15 (m, 1H), 2.22 - 2.13 (m, 1H), 1.83 - 1.70 (m, 2H), 1.64 - 1.52 (m, 3H), 1.51 - 1.43 (m, 2H), 1.42 - 1.34 (m, 1H), 1.04 - 0.92 (m, 1H), 0.89 - 0.77 (m, 1H). LC-MS (ESI⁺) m/z 463.2 (M+H)⁺.

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References

• Mdm2 degraders and uses thereofPublication Number:WO-2023049790-A2Priority Date:2021-09-22
• Mdm2 degraders and uses thereofPublication Number:US-2024025878-A1Priority Date:2020-03-19
• Mdm2 degraders and uses thereofPublication Number:WO-2021188948-A1Priority Date:2020-03-19
• Methods of treating cancerPublication Number:WO-2023114933-A1Priority Date:2021-12-15
• Methods of treating cancerPublication Number:US-2023233546-A1Priority Date:2021-12-15
• Methods of treating cancerPublication Number:CN-118574613-APriority Date:2021-12-15
• Methods of treating cancerPublication Number:EP-4447959-A1Priority Date:2021-12-15
• Mdm2 degraders and uses thereofPublication Number:EP-4405359-A2Priority Date:2021-09-22
• Mdm2 degraders and uses thereofPublication Number:WO-2025096262-A1Priority Date:2023-11-01
• Mdm2 degraders and uses thereofPublication Number:WO-2024197219-A1Priority Date:2023-03-22
• Mdm2 degraders and uses thereofPublication Number:WO-2024197216-A2Priority Date:2023-03-22
• Mdm2 degraders and uses thereofPublication Number:US-2025352535-A1Priority Date:2022-06-06
• Mdm2 degraders and uses thereofPublication Number:WO-2023239697-A1Priority Date:2022-06-06

///////////////////seldegamadlin, anax labs, E3 ubiquitin-protein ligase Mdm2 (Hdm2) degrader, antineoplastic, KT 253, KT-253, VNP2BV6KGL

#seldegamadlin, #anax labs, #E3 ubiquitin-protein ligase Mdm2 (Hdm2) degrader, #antineoplastic, #KT 253, #KT-253, #VNP2BV6KGL

Secutrelvir

 

Secutrelvir

CAS 2996148-73-1

MF C23H16Cl2F3N5O2 MW522.3 g/mol

2-[5-(3-chloro-4-fluorophenyl)-3-(5-chloro-3-pyridinyl)-6-(6,6-difluoro-2-azaspiro[3.3]heptan-2-yl)-2,4-dioxopyrimidin-1-yl]acetonitrile

2-(5-(3-chloro-4-fluorophenyl)-3-(5-chloropyridin-3-yl)-6-(6,6-difluoro-2-azaspiro[3.3]heptan-2-yl)-2,4-dioxo-3,4-dihydropyrimidin-1(2H)-yl)acetonitrile

[5-(3-chloro-4-fluorophenyl)-3-(5-chloropyridin-3-yl)-6-(6,6-difluoro-2-azaspiro[3.3]heptan-2-yl)-2,4-dioxo-3,4-dihydropyrimidin-1(2H)-yl]acetonitrile

[5-(3-chloro-4-fluorophenyl)-3-(5-chloropyridin-3-yl)-6-(6,6-difluoro-2-azaspiro[3.3]heptan-2-yl)-2,4-dioxo-3,4-dihydropyrimidin-1(2H)-yl]acetonitrile
protease inhibitor, antiviral, S-892216, S 892216, FMV68MJ8XK

Secutrelvir (also known by its developmental code S-892216) is an advanced, next-generation oral antiviral drug developed by the pharmaceutical company Shionogi. It functions as a potent SARS-CoV-2 3C-like protease (3CLpro / \(M^{\text{pro}}\)) inhibitor designed primarily for the treatment of COVID-19.

As of August 2026, the drug has entered late-stage development, with Shionogi moving into Phase 3 clinical trials to assess its efficacy and safety in patients.

Key Properties & Advantages

Unlike first-generation COVID-19 antivirals, secutrelvir was structurally optimized to address the limitations of existing treatments like Paxlovid (nirmatrelvir/ritonavir) and Shionogi’s own Xocova (ensitrelvir).

• No CYP Booster Required: Secutrelvir offers 100% oral bioavailability without needing a pharmacokinetic booster like ritonavir. This dramatically reduces the risk of severe drug-drug interactions that complicate Paxlovid prescriptions.
• Overcoming Viral Resistance: In laboratory assays, the compound demonstrates zero cross-resistance to viral mutants that have grown resistant to nirmatrelvir or ensitrelvir (such as those carrying E166V or M49L mutations).
• High Off-Target Selectivity: It features high selectivity (>15,000-fold) over human proteases, ensuring it specifically targets viral replication without disrupting normal human cellular functions.
• Broad Spectrum (Pan- β-CoV): The compound maintains high potency against a wide range of SARS-CoV-2 variants—including newer strains like Omicron JN.1—as well as other coronaviruses like SARS-CoV and MERS-CoV.

---

Mechanism of Action

Secutrelvir relies on a structure-based design incorporating a nitrile warhead. It enters the catalytic active site of the virus's main protease (\(M^{\text{pro}}\)) and forms a reversible covalent bond with the catalytic amino acid residue cysteine C145. By binding to this pocket, it halts the protease from cutting viral polyproteins, effectively stopping viral replication in its tracks.

[Secutrelvir (Nitrile Warhead)] 
           │
           ▼ (Reversible Covalent Binding)
   [Cysteine C145 of 3CLpro] ──► Blocked Protease Activity ──► Viral Replication Stopped

---

Clinical Evaluation Status

• Pharmacokinetics: Clinical pharmacology data released by Shionogi Medical demonstrated excellent safety, high tolerability, and no clinically relevant food effects, meaning the drug can be taken with or without food.
• Phase 3 Trials (NCT07743580 / NCT07746544): Late-stage double-blind, placebo-controlled interventional studies are assessing the drug in symptomatic, non-hospitalized COVID-19 patients who are at risk of progressing to severe illness. To qualify for the trials, patients must receive the drug within 72 hours of symptom onset

• A Study of Secutrelvir in Participants With Coronavirus Disease 2019 (COVID-19) Who Are at High Risk for Progression to Severe DiseaseCTID:NCT07743580Phase:Phase 3Status:RecruitingDate:2026-08-25
• Study of Secutrelvir in Participants With COVID-19CTID:NCT07746544Phase:Phase 3Status:Not yet recruitingDate:2026-08-05
• A Study of S-892216 in Participants With COVID-19CTID:NCT06928051Phase:Phase 2Status:CompletedDate:2025-09-30
• A Drug-drug Interaction Study of S-892216 Coadministered With Carbamazepime to Healthy Adult ParticipantsCTID:NCT06751017Phase:Phase 1Status:CompletedDate:2025-03-11

Syn

US20250092056,

https://patentscope.wipo.int/search/en/detail.jsf?docId=US451712998&_cid=P20-MTTHQ4-21870-1

Example 6

Synthesis of Compound (I-077)

Step 1 Synthesis of Compound (I-077)

Compound (I-055) (25.0 mg, 0.059 mmol), 6,6-difluoro-2-azaspiro[3.3]heptane trifluoroacetic acid salt (17.4 mg, 0.070 mmol), N, N-diisopropylethylamine (20.5 μL, 0.117 mmol), and DMF (0.5 mL) were mixed, and the solution was stirred at 60° C. for 2 hours. Water (2 mL) was added to the reaction solution, and the mixture was extracted with ethyl acetate. The organic layer was washed with water, dried over sodium sulfate, and filtered. The filtrate was concentrated, and ethyl acetate (0.05 mL), hexane (0.125 mL), and diisopropyl ether (0.125 mL) were added. The obtained precipitate was collected by filtration and washed with diisopropyl ether. The obtained solid was dried under reduced pressure to obtain Compound (I-077) (22.0 mg, 0.042 mmol, yield 72%).

1H-NMR (CDCl 3) δ: 2.75 (4H, t, J=12.0 Hz), 4.02 (4H, s), 4.74 (2H, s), 7.16-7.18 (2H, m), 7.32-7.35 (1H, m), 7.65 (1H, t, J=2.1 Hz), 8.43 (1H, d, J=2.3 Hz), 8.61 (1H, d, J=2.3 Hz).

LC/MS (ESI): m/z=522, RT=2.27 min, LC/MS measurement condition A

PAT

[WO2023195530A1]

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AS ON FEB2026 4.574 LAKHS VIEWS ON BLOG WORLDREACH AVAILABLEFOR YOUR ADVERTISEMENT

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References

Uracil derivatives having virus replication inhibitory activity and pharmaceutical composition comprising the samePublication Number:

US-2025092056-A1Priority Date:2022-04-08

////secutrelvir, anax labs, protease inhibitor, antiviral, S-892216, S 892216, FMV68MJ8XK

#secutrelvir, #anax labs, #protease inhibitor, #antiviral, #S-892216, #S 892216, #FMV68MJ8XK

Rugocrixan

 

Rugocrixan

CAS911715-90-7

MF C19H25N5OS2, MF 403.6 g/mol

(2R)-2-[[2-amino-5-[(1S)-1-phenylethyl]sulfanyl-[1,3]thiazolo[4,5-d]pyrimidin-7-yl]amino]-4-methylpentan-1-ol

1-Pentanol, 2-[[2-aMino-5-[[(1S)-1-phenylethyl]thio]thiazolo[4,5-d]pyriMidin-7-yl]aMino]-4-Methyl-, (2R)-

(R)-2-((2-Amino-5-(((S)-1-phenylethyl)thio)thiazolo[4,5-d]pyrimidin-7-yl)amino)-4-methylpentan-1-ol

(2R)-2-[(2-amino-5-{[(1S)-1-phenylethyl]sulfanyl}[1,3]thiazolo[4,5-d]pyrimidin-7-yl)amino]-4-methylpentan-1-ol
CX3C chemokine receptor 1 (CX3CR1) antagonist, antiinflammatory, KAND567, AZD8797, KAND 567, AZD 8797, S9Y83SS7PQ

Rugocrixan (also known by its developmental codes KAND567 and AZD8797) is a first-in-class, orally active small molecule drug candidate developed by Novakand Pharma (formerly Kancera). It acts as a potent, non-competitive allosteric antagonist of the CX3CR1 receptor, which is commonly referred to as the fractalkine receptor. By blocking this specific pathway, the drug prevents hyperinflammation and inhibits the proliferation and DNA repair mechanisms of certain cancer cells.

KAND567, a small molecule, blocks the fractaline (CX3CL1) receptor, which mediates the immune system response to inflammation. Because COVID-19 involves cytotoxic cells associated with this pathway, KAND567 is currently being tested as a treatment for those with the illness.

KAND567, a small molecule, blocks the fractaline (CX3CL1) receptor, which mediates the immune system response to inflammation. Because COVID-19 involves cytotoxic cells associated with this pathway, KAND567 is currently being tested as a treatment for those with the illness.

Key Clinical Developments and Therapeutic Focus

Originally acquired from AstraZeneca, the drug has advanced into multiple Phase II clinical trials. Novakand Pharma transitioned its core business strategy to focus heavily on orphan drug designations for niche, treatment-resistant conditions. Its primary areas of investigation include:

• Ovarian Cancer: Evaluated in the Phase IIa "KANDOVA" clinical trial for patients with treatment-resistant ovarian cancer. It functions by suppressing DNA repair in tumor cells, which enhances the effectiveness of platinum-based chemotherapy and drives the cancer cells into programmed cell death.
• Hematological Cancers: In preclinical studies alongside institutions like the Karolinska Institutet, rugocrixan has demonstrated a capability to block the unwanted growth-promoting effects of immune cells on advanced blood cancers, such as chronic lymphocytic leukemia (CLL).
• Cardioprotection: Investigated via the "FRACTAL" Phase IIa trial in patients suffering from acute myocardial infarction (STEMI) undergoing angioplasty. The drug met its safety endpoints and showed signals of protecting heart tissue by reducing myocardial bleeding and the risk of thrombosis.

Companion Prodrug

Novakand Pharma is also developing a second-generation, water-soluble phosphate prodrug named fosrugocrixan (KAND145). Once administered, fosrugocrixan is metabolized into the active form of rugocrixan, offering enhanced product properties for intravenous or alternative delivery methods.

Because rugocrixan targets a brand-new pharmacological pathway, the World Health Organization (WHO) assigned it a unique suffix stem, establishing it as the international nomenclature standard for this entire new class of CX3CR1 antagonists

• A Study to Evaluate the Safety of KAND567, in Combination With Carboplatin Therapy, in Women With Recurrent Epithelial Ovarian, Fallopian Tube, or Primary Peritoneal CancerCTID:NCT06087289Phase:Phase 1/Phase 2Status:CompletedDate:2025-06-08
• Safety, Tolerability and Pharmacokinetics After Continuous Infusion of KAND567CTID:NCT06030375Phase:Phase 1Status:CompletedDate:2023-09-11
• KAND567 Versus Placebo in Subjects Hospitalized With COVID-19CTID:NCT06012565Phase:Phase 2Status:TerminatedDate:2023-08-25
• KANDOVA - A two-part Phase Ib/IIa study to evaluate the safety and tolerability of KAND567, in combination with carboplatin therapy, and to determine the Recommended Phase II Dose (RPIID) of KAND567. An open-label, multicenter dose escalation study with an expansion cohort in women with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer.EudraCT:2022-002792-11Phase:Phase 2Status:Trial now transitionedDate:2023-03-27
• KAND567 Versus Placebo in Subjects Hospitalized with COVID-19. A Phase II, Randomized, 2-Arm Parallel-Group, Double-blind Study to Evaluate Efficacy, Safety, Tolerability, and Pharmacokinetics.EudraCT:2020-002322-85Phase:Phase 2Status:Completed, Prematurely EndedDate:2020-07-02

SYN

compound 18a [PMID: 23516963]

PAT

WO 2006/107258.

PAT

EP1869056

https://patentscope.wipo.int/search/en/detail.jsf?docId=EP14857146&_cid=P20-MTP714-98881-1

Example 12

(2R)-2-[{2-Amino-5-[(1-phenylethyl)thio][1,3]thiazolo[4,5-d]pyrimidin-7-yl}(methyl)amino]-4-methylpentan-1-ol

a) (2R)-2-[[2-Amino-5-(benzylthio)[1,3]thiazolo[4,5-d]pyrimidin-7-yl](methyl)amino]-4-methylpentan-1-ol

[0097]  5-(Benzylthio)-7-chloro[1,3]thiazolo[4,5 -d]pyrimidin-2-amine (1.5 g, 4.86 mmol), DIPEA (691 mg, 5.35 mmol) and ( R)- N-methylleucinol (956 mg, 7.29 mmol) were mixed in NMP (7.5 mL). The resulting solution was stirred at 110 °C under a nitrogen atmosphere for 2 days. After cooling to room temperature the reaction mixture was poured onto ice. The resulting yellow precipitate was collected by filtration, washed with water and dried in vacuo. The crude product was purified by flash column chromatography on silica (DCM:EtOAc 50:50 to 0:100) to give 1.42 g (72% yield) of the title compound as a yellow solid.
¹H NMR (DMSO-d ₆) 7.97 (br s, 2H), 7.40 (m, 2H), 7.28 (m, 2H), 7.21 (m, 1H), 4.73 (dd, 1H), 4.64 (br s, 1H), 4.32 (br s, 2H), 3.52-3.37 (m, 2H), 3.00 (s, 3H), 1.55-1.35 (m, 2H), 1.27 (m, 1H), 0.88 (d, 3H), 0.80 (d, 3H);
MS (ESI ⁺) m/ z 404 [M+H] ⁺.

PAT

RU0002411245

PAT

WO2019219771

https://patentscope.wipo.int/search/en/detail.jsf?docId=WO2019219771&_cid=P20-MTP714-98881-2

(2R)-2-[(2-amino-5-{[(1S)-1- phenylethyl]thio}[1 ,3]thiazolo[4,5-c/]pyrimidin-7-yl)amino]-4-methylpentan-1-ol is known to be a potent antagonist .

3.4 Preparation of (2R)-2-r(2-amino-5-(r(1 S)-1 -phenylethyllthio)ri ,3lthiazolor4,5-c/1Pyrimidin-7-yl)aminol-4-methylpentan-1 -ol.xHCI (5)

.xHCI

Compound 4 (1 .852 g, 5.74 mmol), DIPEA (1.1 12 g, 8.61 mmol) and D-leucinol (1.008 g, 8.61 mmmol) were dissolved in NMP (12 ml.) and the mixture was stirred at 120 °C in a sealed pyrex tube (start: 17:40).

HPLC after 15.5 h: ca. 98% conversion

HPLC after 19.5 h: >99% conversion

Work up: Ice water was poured into the mixture. Initially a solid was formed, but at the end of the addition the solid collapsed to a dark brown oil. EtOAc (50 ml.) was added and the phases were separated. The aqueous phase was extracted with EtOAc (2x25 ml_), and the combined organic phases were washed with water (8 ml_), sat. NaHC03 (3x8 ml_), water (8 ml.) and brine (8 ml_), dried over MgS04, filtered and evaporated. Dried in vacuum to yield 2.697 g of crude material as a brown oil. HPLC purity: ca. 92%. The oil was dissolved in MEK (ca. 18 mL) and cone. HCI (12.5 M, 574 pL, 7.18 mmol) was added. There was no spontaneous precipitation of the HCI salt. The mixture was gently stirred at RT and after ca. 20 min precipitation occurred. The mixture was stirred gently for 2.5 h and the solid was isolated by filtration on a P3 sintered glass filter. The solid was washed with three portions of MEK and was then dried in vacuum at 60 °C for 2.5 days. Yield (batch 1 ): 1 .224 g (48.5%) of the product as hydrochloride salt.

HPLC purity: 99.0% (basic method);

97.4% (acidic method).

A substantial amount of solids passed through the filter into the filtrate. The solids were isolated by centrifugation and the supernatant was removed by pipette. The solid was washed with two portions (ca. 2x5 mL) of MEK. After the last supernatant was removed the product was dried in vacuum at 60 °C for 2.5 days. Yield (batch 2): 324 mg (12.8%) of the product as hydrochloride salt.

HPLC purity: 99.0% (basic method);

97.5% (acidic method).

Combined yield: 1.548 g (61 .3%)

Both batches contain ca. 0.07% DMF (w/w). The DMF was already present in the starting material.

Further purification of the combined batches

The two batches of compound 5 were combined (1.338 g, 3.041 mmol) in a 50 mL roundbottomed flask and water (6 mL) was added followed by 2M NaOH (1.6 mL, 3.2 mmol). The mixture was stirred and EtOAc (40 mL) was added. An additional 0.5 mL (1 mmol) 2M NaOH was added during stirring. After 15 min all of the solids were dissolved and the phases were separated. The pH of the aqueous phase was measured with a pH stick =>pH=7. More 2M NaOH (0.4 mL, 0.8 mmol) was added to the aqueous phase resulting in a pH of 10. The aq. phase was extracted with EtOAc (25 mL) and the phases were separated. The combined organic phases were dried over Na₂S0₄, filtered and evaporated to yield the free base as a crystalline beige solid. The free base was dissolved in MEK (15 mL) and HCI (37%, 12.5 M, 255 pL, 3.19 mmol) was added during stirring. A white precipitate was immediately formed. The mixture was stirred gently for 2 h and the solid was collected by filtration on a P4 sintered glass filter. The solids were washed with MEK (5 mL) and dried in vacuum at 60 °C for 3 h. Yield: 1.187 g (89% based on the unpurified material) of 99% pure product as a white solid. ¹H NMR (600 MHz, CD30D) d ppm 7.49 (d, J=7.3 Hz, 2 H) 7.37 (t, J=7.6 Hz, 2 H) 7.27 - 7.32 (m, 1 H) 5.23 (q, J=7.0 Hz, 1 H) 4.60 - 4.70 (m, 1 H) 3.55 (d, J=5.5 Hz, 2 H) 1.83 (d, J=7.3 Hz, 3 H) 1.67 - 1.76 (m, 1 H) 1.58 -1.65 (m, 1 H) 1.48 - 1.54 (m, 1 H) 1.00 (d, J=6.7 Hz, 3 H) 0.98 (d,J=6.7 Hz, 3 H). MS (ESI+) m/z 404 [M+H]⁺

The diasteromeric ratio of the final product reflects the enantiomeric ratio of the starting material (compound 1 ), which was 99.7% (S).

¹H NMR: The spectrum looks very pure. Trace amounts of DMF were, however, detected.

Comparative Example 4 - Process scale two-step procedure for the synthesis of 6-amino-2-{r(1S)-1-phenylethvnsulfanyl)pyrimidin-4-ol (1 )

Step 1 Step 2

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References

• Novel 5-substituted 7-amino-[1,3]thiazolo[4,5-d]pyrimidine derivativesPublication Number:CA-2604017-CPriority Date:2005-04-06Grant Date:2012-03-06
• Novel 5-substituted 7-amino [1,3] thiazolo [4,5-D] pyrimidine derivativesPublication Number:JP-5165553-B2Priority Date:2005-04-06Grant Date:2013-03-21
• Novel 5,7-Disubstituted [1,3]Thiazolo[4,5-D]Pyrimidin-2(3H)-One Derivatives 794Publication Number:US-2009124637-A1Priority Date:2005-04-06
• New derivatives of 5, 7-disubstituted [1, 3] thiazolo[4, 5-d] pyrimidine-2(3h)-onePublication Number:RU-2411245-C9Priority Date:2005-04-06Grant Date:2011-05-27
• Novel 5-Substituted 7-Amino-[1,3]Thiazolo[4,5-D]Pyrimidine Derivatives 793Publication Number:US-2008214578-A1Priority Date:2005-04-06
• NEW DERIVATIVES OF 5-SUBSTITUTED 7-AMINO-[1, 3] THIAZOLO [4, 5-d]PYRIMIDINEPublication Number:RU-2419623-C2Priority Date:2005-04-06Grant Date:2011-05-27
• Novel 5,7-disubstituted [1,3] thiazolo [4,5-D] pyrimidin-2 (3H) -one derivativesPublication Number:JP-2008535834-APriority Date:2005-04-06

//////////rugocrixan, anax labs, CX3C chemokine receptor 1 (CX3CR1) antagonist, antiinflammatory, KAND567, AZD8797, KAND 567, AZD 8797, S9Y83SS7PQ

#rugocrixan, #anax labs, #CX3C chemokine receptor 1 (CX3CR1) antagonist, #antiinflammatory, #KAND567, #AZD8797, #KAND 567, #AZD 8797, #S9Y83SS7PQ

Romaciclib

 

Romaciclib

CAS 1609522-33-9

MWC15H18Br2N4 MF414.14 g/mol

6,7-dibromo-5-methyl-2-piperazin-1-yl-1,3-diazatricyclo[6.3.1.0^4,12]dodeca-2,4,6,8(12)-tetraene

7,8-dibromo-9-methyl-2-(piperazin-1-yl)-5,6-dihydro-4Himidazo[4,5,1-ij]quinoline
cyclin-dependent kinase inhibitor, antineoplastic, RVU-120, SEL-120, SEL120-34, SEL120-34A, RVU 120, SEL 120, ORPHAN DRUG, 6LGR0RYY5Q

Romaciclib is an investigational new drug being evaluated by Ryvu Therapeutics for the treatment of acute myeloid leukaemia (AML). It is a dual inhibitor of CDK8 and CDK19.^[1][2][3]

Romaciclib is an investigational, orally bioavailable small-molecule dual inhibitor of cyclin-dependent kinases 8 and 19 (CDK8 and CDK19), being developed by Ryvu Therapeutics for the treatment of hematologic malignancies such as acute myeloid leukemia (AML) and myelofibrosis.

Mechanism of Action

• Targeted Inhibition: Romaciclib selectively targets CDK8 and CDK19 to disrupt oncogenic transcription programs essential for cancer cell survival while minimizing off-target effects.
• Oral Administration: As an oral pill, it offers convenience and supports long-term therapy compliance compared to intravenous treatments.
• Combination Potential: Preclinical and clinical evaluations show it helps overcome resistance mechanisms—such as restoring sensitivity to venetoclax (VEN) in relapsed/refractory AML—and exhibits synergistic activity with JAK inhibitors in myelofibrosis models.

Clinical Development

• Acute Myeloid Leukemia (AML): Evaluated in the Phase II RIVER-81 study in combination with venetoclax, showing encouraging anti-leukemic activity and durable responses in patients with relapsed or refractory disease.
• Myelofibrosis (MF): Investigated as a monotherapy or combined with ruxolitinib in the Phase II POTAMI-61 trial

• RVU120 Rollover StudyCTID:NCT06987058Phase:Phase 2Status:Enrolling by invitationDate:2026-07-28
• RVU120 in Patients With Intermediate or High-risk, Primary or Secondary MyelofibrosisCTID:NCT06397313Phase:Phase 2Status:RecruitingDate:2025-09-23
• RVU120 for Treatment of Anemia in Patients With Lower-risk Myelodysplastic NeoplasmsCTID:NCT06243458Phase:Phase 2Status:Active, not recruitingDate:2025-05-22
• Safety and Efficacy of RVU120 for Treatment of Relapsed/Refractory AMLCTID:NCT06268574Phase:Phase 2Status:Active, not recruitingDate:2025-05-08
• Safety and Efficacy of RVU120 Combined With Venetoclax for Treatment of Relapsed/Refractory AMLCTID:NCT06191263Phase:Phase 2Status:RecruitingDate:2025-04-13

• OriginatorSelvita
• DeveloperRyvu Therapeutics
• ClassAntineoplastics; Halogenated hydrocarbons; Imidazoles; Piperazines; Quinolones; Small molecules
• Mechanism of ActionCyclin dependent kinase 19 inhibitors; Cyclin-dependent kinase 8 inhibitors
• Orphan Drug StatusYes - Acute myeloid leukaemia
• Phase IIAcute myeloid leukaemia; Myelodysplastic syndromes; Myelofibrosis; Solid tumours
• Phase IMedulloblastoma
• 11 Jun 2026The US FDA reactivates the IND, enabling the initiation of the expansion cohort of phase II RIVER-81 trial in Acute myeloid leukaemia at the recommended dose of 150 mg once daily (QD)
• 11 Jun 2026Updated efficacy data from a phase II RIVER-81 trial in Acute myeloid leukaemia released by Ryvu Therapeutics
• 21 May 2026Ryvu Therapeutics plans a phase II ROVER-01 trial for Acute myeloid leukaemia, Myelodysplastic syndromes and Solid tumours in the Poland and Spain (NCT06987058)

Romaciclib is an orally bioavailable inhibitor of cyclin-dependent kinases 8 and 19 (CDK8/19), with potential antineoplastic and chemoprotective activities. Upon oral administration, romaciclib targets, binds to and inhibits the activity of CDK8/19, which prevents activation of CDK8/19-mediated oncogenic signaling pathways, blocks selective transcription of various tumor-promoting genes, and inhibits proliferation of CDK8/19-overexpressing tumor cells. CDK8/19, serine/threonine kinases involved in the regulation of the cell cycle, are overexpressed in certain cancer cell types and play key roles in tumor cell proliferation.

PAT

US20150274726

https://patentscope.wipo.int/search/en/detail.jsf?docId=US152387110&_cid=P10-MTMCT7-27170-1

7,8-dibromo-9-methyl-2-(piperazin-1-yl)-5,6-dihydro-4H-imidazo[4,5,1-ij]quinoline,

PAT

• Substituted tricyclic benzimidazoles as kinase inhibitorsPublication Number:EP-2917217-B1Priority Date:2012-11-08Grant Date:2017-03-08
• Substituted tricyclic benzimidazoles as kinase inhibitorsPublication Number:CN-104903321-APriority Date:2012-11-08
• SUBSTITUTED TRICYCLIC BENZIMIDAZOLS, THEIR USES, AND PHARMACEUTICAL COMPOSITIONPublication Number:BR-112015010019-B1Priority Date:2012-11-08
• Substituted tricyclic benzimidazoles as kinase inhibitorsPublication Number:US-9745299-B2Priority Date:2012-11-08Grant Date:2017-08-29
• Substituted tricyclic benzimidazoles as kinase inhibitorsPublication Number:US-2015274726-A1Priority Date:2012-11-08
• C. novyi for the treatment of solid tumors in humansPublication Number:EP-3730146-B1Priority Date:2013-03-29Grant Date:2022-05-04
• Clostridium nodarii for the treatment of human solid tumorsPublication Number:CN-105451750-BPriority Date:2013-03-29Grant Date:2023-03-10
• C. novyi for the treatment of solid tumors in humansPublication Number:EP-4108248-A1Priority Date:2013-03-29
• C. novyi for the treatment of solid tumors in non-human animalsPublication Number:US-12433920-B2Priority Date:2013-03-29Grant Date:2025-10-07
• C. novyi for the treatment of solid tumors in humansPublication Number:EP-4108248-B1Priority Date:2013-03-29Grant Date:2025-09-17

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#MedicinalChemistry, #DrugDiscovery, #OrganicSynthesis, #ChemicalLibrary, #BuildingBlocks, #SARStudies, #ChemistryInnovation, #medchem, #Drugdevelopment, #Biotech, #Biotechnology, #AnaxLaboratories, #Pharma

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References

1.  "Romaciclib - Ryvu Therapeutics". AdisInsight. Springer Nature Switzerland AG.
2.  Rajendra A, Yee KW (April 2026). "Clinical development of a CDK8/19 kinase inhibitor for acute myeloid leukemia". Expert Opinion on Investigational Drugs. 35 (4): 253–256. doi:10.1080/13543784.2026.2656430. PMID 41931045.
3.  Pakulska U, Obacz M, Woźnicki J, Wiklik K, Chakraborty S, Micek M, et al. (January 2026). "Romaciclib, a CDK8/CDK19 inhibitor, can overcome venetoclax resistance through a combinatorial strategy". bioRxiv 10.64898/2025.12.16.693978.

• Cyclin-Dependent Kinase 8: A New Hope in Targeted Cancer Therapy?Publication Name:Journal of Medicinal ChemistryPublication Date:2017-12-21PMID:29266937DOI:10.1021/acs.jmedchem.7b00901
• SEL120-34A is a novel CDK8 inhibitor active in AML cells with high levels of serine phosphorylation of STAT1 and STAT5 transactivation domainsPublication Name:OncotargetPublication Date:2017-04-04PMCID:PMC5464911PMID:28422713DOI:10.18632/oncotarget.16810

• Discovery of a Novel and Potent Cyclin-Dependent Kinase 8/19 (CDK8/19) Inhibitor for the Treatment of CancerPublication Name:Journal of Medicinal ChemistryPublication Date:2024-05-01PMID:38690856DOI:10.1021/acs.jmedchem.4c00248
• Discovery of a novel oral type Ⅰ CDK8 inhibitor against acute myeloid leukemiaPublication Name:European Journal of Medicinal ChemistryPublication Date:2023-05-05PMID:36889252DOI:10.1016/j.ejmech.2023.115214
• Discovery of Potent, Selective, and Orally Bioavailable Small-Molecule Inhibitors of CDK8 for the Treatment of CancerPublication Name:Journal of Medicinal ChemistryPublication Date:2023-04-07PMID:37029334DOI:10.1021/acs.jmedchem.2c01718
• From Structure Modification to Drug Launch: A Systematic Review of the Ongoing Development of Cyclin-Dependent Kinase Inhibitors for Multiple Cancer TherapyPublication Name:Journal of Medicinal ChemistryPublication Date:2022-04-29PMID:35485642DOI:10.1021/acs.jmedchem.1c02064
• A comprehensive insight on the recent development of Cyclic Dependent Kinase inhibitors as anticancer agentsPublication Name:European Journal of Medicinal ChemistryPublication Date:2020-10-01PMID:32707525DOI:10.1016/j.ejmech.2020.112571

//////////romaciclib, ANAX LABS, cyclin-dependent kinase inhibitor, antineoplastic, RVU-120, SEL-120, SEL120-34, SEL120-34A, RVU 120, SEL 120, ORPHAN DRUG, 6LGR0RYY5Q

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