Patent SAR Analysis Indole-substituted Quinolines LS174T · c-MYC Hot R&D Patent

US20240300921A1 — Indole-substituted Quinolines + Plk1 Inhibitor SAR

A focused 40-compound library of 2-aminoquinoline analogs evaluated against LS174T colon cancer cells, with a headline Plk1 combination synergy claim. This page presents the complete 95-record SAR readout, multi-dimensional descriptor profile, and 211 activity-cliff comparisons — auto-extracted from the patent by Eureka LS.

SAR Data Records
95records · 40 compounds
Source: Patent Table 3, page 31
Top Inhibition Rate
99.8% @ 3 µM
LMK-5-67 · phenyl-thiazole + N(Me)2
Plk1 Combination Synergy
10.56Bliss score
ISQ-1 + BI2536, well above +5 threshold
Dose Range Tested
62 nM– 3 µM
5-level dose-response, 5-day endpoint

Indole-substituted quinolines (ISQs) sit at the intersection of two long-standing oncology chemotypes — the quinoline scaffold familiar from kinase inhibitors and the indole pharmacophore central to a generation of anti-proliferative agents. Patent US20240300921A1 formalises a focused library of 40 such compounds and pairs them with a Plk1 inhibitor combination claim, framing the series as a treatment for c-MYC-driven cancers.

This page presents the full SAR readout of the patent in a single, navigable view: every compound code, every dose-response point, the multi-dimensional descriptor profile, and the most informative activity-cliff comparisons — all extracted automatically by Eureka LS. The aim is to make the patent's chemistry searchable rather than locked inside a 60-page PDF.

Section 01 · Patent overview

What the patent claims, in one paragraph.

Indole-substituted quinolines presented as anti-proliferative agents for c-MYC-driven cancers, optionally combined with a polo-like kinase 1 (Plk1) inhibitor.

The disclosure covers a series of 2-aminoquinolines bearing an indole, benzofuran, benzothiazole, or thiazole substituent at the 3-position, and a basic amine — most commonly N(Me)2, NHMe, piperidine, piperazine, pyrrolidine, or morpholine — at the 7-position. The shared scaffold is captured by the SMARTS pattern Nc1nc(cc(cc2)[R2])c2cc1[R1], which matches every one of the 40 disclosed analogs.

Activity is measured as cell-proliferation inhibition in LS174T colon-cancer cells (a c-MYC-driven CRC model), assayed via culture-medium addition over a 5-day endpoint. Doses span four orders of magnitude — 62 nM, 125 nM, 250 nM, 500 nM, 1 µM and 3 µM — and several compounds appear at multiple doses, giving partial dose-response curves rather than single-point screens.

The patent's distinguishing therapeutic claim is the combination with a Plk1 inhibitor. Co-dosing the lead compound ISQ-1 with BI2536 (a clinical Plk1 inhibitor) yields a Bliss synergy score of 10.56, comfortably above the +5 threshold that conventionally separates synergy from additivity.

Patent at a glance
95
SAR data points
across 40 unique compounds
99.8%
Top inhibition
LMK-5-67 @ 3 µM
10.56
Bliss synergy
ISQ-1 + BI2536
62 nM
Lowest dose tested
5-level dose-response
3.3 – 6.0
CLogP range
oral-bioavailable space
2 / 40
Mutagenicity flags
p-OMe-benzothiazoles

Compound nomenclature

The patent uses three internal code prefixes that group analogs by synthetic series:

  • ISQ-n (ISQ-1 through ISQ-10) — the named lead series, primarily 1-methylindole-substituted quinolines with varied 7-position amines.
  • VMS-n-m (e.g. VMS-7-7, VMS-8-67) — a synthetic exploration series including benzofuran, benzothiazole, and dichlorophenyl R1 variants.
  • LMK-n-m (e.g. LMK-5-67, LMK-6-89) — the largest series, covering thiazole-aryl, fluorophenyl, and modified piperidine R2 variants.
Section 02 · Key findings

Five things the SAR data tells us.

Distilled from the full 95-record dataset and the multi-dimensional descriptor profile.

Finding 01
A single 2-aminoquinoline scaffold underpins the entire 40-compound library.
Every disclosed analog matches Nc1nc(cc(cc2)[R2])c2cc1[R1]. SAR variation is concentrated at two positions: R1 (a heteroaryl on quinoline-3) and R2 (a basic amine on quinoline-7). This makes the patent unusually clean to triage — the chemistry space is small and well-defined.
Finding 02
R2 amine basicity drives sub-µM potency more than R1 identity.
At 3 µM nearly half the library reaches >90% inhibition regardless of R1. Below 250 nM, the picture flips: only compounds carrying basic, sp³-rich R2 amines (1-Me-piperazine in ISQ-3, 4-pyridyl-piperidine in ISQ-10, methoxymethyl-piperidine in ISQ-9) retain >95% inhibition. R1 modulates the Hill slope; R2 sets the IC50.
Finding 03
The combination with Plk1 surfaces as the strongest activity cliff.
ISQ-1 alone is moderate at 250 nM (~38% inhibition). ISQ-1 + BI2536 produces a Bliss synergy of 10.56 against LS174T — one of the largest deltas in the dataset. The patent's combination claim is therefore not incidental; it is empirically the most differentiated readout in the disclosure.
Finding 04
All 40 analogs sit inside oral-bioavailable physicochemical space.
CLogP 3.31 – 6.03; TPSA 42 – 93 Ų; molecular weight uniformly < 500 Da. Two compounds (LMK-5-62, LMK-5-68) carry high mutagenicity flags, both featuring a p-methoxy benzothiazole — a known structural alert that should be prioritised for de-risking.
Finding 05
Top-of-class candidates concentrate in the LMK-5 and ISQ-10 sub-series.
LMK-5-67 (99.8% @ 3 µM, phenyl-thiazole + N(Me)2) and ISQ-10 (99% @ 250 nM, pyridyl-piperidine) anchor opposite ends of the lead-finding strategy: highest-potency single-shot vs. lowest-dose efficacy. Either is a credible starting point depending on whether the program prioritises potency or dose flexibility.
"Out of 95 measurements, the most informative single number is not the best inhibition — it is the Bliss synergy of 10.56 between ISQ-1 and BI2536." — Eureka LS, automated SAR analysis of US20240300921A1
Try it on your own patent

Start extracting patent SAR data — input any patent number, get a structured dataset in under 30 seconds.

Built for drug-discovery researchers who need to triage IP fast. Eureka LS handles USPTO, EPO, WIPO and CNIPA.

US20240300921A1 WO2025189057A1 EP4123456A1 CN115784986B
Section 03 · Full SAR dataset

95 activity records, 40 compounds, one cell line.

Below is a top-activity preview from the full extraction. The complete dataset — including every dose-response point, SMILES, dosing regimen, and source-page citation — is available in Eureka LS.

The patent reports cell-proliferation inhibition for 40 unique compounds, evaluated at up to six different concentrations each, yielding 95 individual activity measurements. Inhibition values range from 2% (LMK-6-99 at 62 nM) to 99.8% (LMK-5-67 at 3 µM). The distribution skews bimodal — 47 records report ≥80% inhibition, 36 report <50%, with relatively few in between — reflecting the dose-response nature of the underlying assay.

Table 1
SAR Activity Data — Top 10 by inhibition rate
95 records total 40 compounds
Compound Subject Indicator Dose Inhibition Activity
Table 1. Top 10 cell-proliferation inhibition values from US20240300921A1 against LS174T colon cancer cells. Activity bands: High ≥ 80%, Moderate 50–79%, Low < 50%. Source: Patent Table 3, page 31; auto-extracted by Eureka LS.
Section 04 · Multi-dimensional overview

Beyond raw activity — the descriptor profile of the series.

Eureka LS auto-computes physicochemical descriptors, druglikeness, ligand efficiency, mutagenicity, and scaffold/ring decomposition for every extracted compound.

The 40 ISQ analogs occupy a tight, well-behaved region of physicochemical space. Lipophilicity (CLogP) ranges from 3.31 to 6.03 — most compounds sit comfortably in the lead-like 3-5 window, with three outliers above 5 that warrant permeability checks. Topological polar surface area is uniformly below the 90 Ų oral-bioavailability threshold, confirming the series is well-suited to oral dosing.

CLogP range
3.31 – 6.03
28/40 compounds in the 3–5 lead-like window. Three outliers (>5) flagged for permeability review.
TPSA range
42 – 93 Ų
All 40 compounds below the 140 Ų oral-bioavailability threshold; mean ≈ 60 Ų.
Druglikeness score
−2.71 → +4.96
31/40 above zero (favorable). Best: ISQ-10 (4.96). Lowest: LMK-5-60 (−2.71).
Mutagenicity (Ames)
38 None · 2 High
Only LMK-5-62 and LMK-5-68 carry high flags — both share a p-OMe benzothiazole motif.
Common scaffold
2-aminoquinoline
Pattern Nc1nc(cc(cc2)[R2])c2cc1[R1] — shared by all 40 analogs.
Ring systems
3 – 4 rings
Quinoline + indole / benzofuran / benzothiazole / thiazole + a piperidine-class amine.

Compound-level descriptor profile

Below is the descriptor breakdown for the 12 most active compounds, the natural starting set for downstream lead optimisation.

Table 2
Multi-dimensional Overview — top 12 compounds by activity
95 records total
Compound Inhibition CLogP TPSA Druglikeness Ames R1, R2 substituents
Table 2. Multi-dimensional descriptor profile for the top-12 most active analogs. CLogP and TPSA computed via standard cheminformatics; druglikeness on a QED-style scale (higher is better); Ames mutagenicity from in-silico Ames model. Source: Eureka LS Multi-dimensional Overview output.
Key observation The two compounds carrying high mutagenicity flags (LMK-5-62, LMK-5-68) both contain a p-methoxy benzothiazole R1 group — a known structural alert. The patent does not address this finding directly. For lead-optimisation prioritisation, switching to LMK-5-66 (4-Br-phenyl thiazole, no flag) preserves >98% inhibition while removing the alert.
Section 05 · Activity-cliff comparisons

The single-bond changes that move the needle.

Activity cliffs — pairs of structurally similar compounds with sharply different activity — pinpoint exactly which substituents drive SAR. Eureka LS auto-generated 211 such pairs across the patent.

Of the 211 pairwise comparisons, 12 qualify as canonical activity cliffs (Tanimoto similarity > 0.85, Δ inhibition > 50%). Five of these are reproduced below — chosen because they isolate one specific design choice each.

Similarity 0.97 Δ Inhibition 2.4% Cliff 1 — N-methylation on quinoline-7 amine · R2 minor variation
ISQ-1
CN(C)C1=CC=C2C=C(C3=CN(C)C4=CC=CC=C34)C(N)=NC2=C1
99.3% @ 3 µM
VMS-8-67
CNC1=CC=C2C=C(C3=CN(C)C4=CC=CC=C34)C(N)=NC2=C1
96.9% @ 3 µM
Reading: Replacing N(Me)2 with NHMe at quinoline-7 has minimal effect on Emax — both compounds saturate near 100% at 3 µM. The choice is therefore one of metabolic profile rather than potency.
Similarity 0.94 Δ Inhibition 89% Cliff 2 — Steep dose-response on ISQ-2 · 8× dose range
ISQ-2 @ 62 nM
CN1C=C(C2=CC=CC=C12)C1=CC2=CC=C(C=C2N=C1N)N1CCCCC1
8.2% @ 62 nM
ISQ-2 @ 500 nM
same compound, dose-escalated
97% @ 500 nM
Reading: The ISQ-2 dose-response is unusually steep — 8% to 97% over an 8× dose range. This Hill behavior is typical of a cooperative or two-hit mechanism, plausibly consistent with the c-MYC-driven proliferation collapse the patent describes.
Similarity 0.94 Δ Inhibition 12% Cliff 3 — 4-cyano vs 4-pyridyl on piperidine
ISQ-7 (4-CN-piperidine)
CN1C=C(C2=CC=CC=C12)C1=CC2=CC=C(C=C2N=C1N)N1CCC(CC1)C#N
19% @ 62 nM
ISQ-10 (4-pyridyl-piperidine)
CN1C=C(C2=CC=CC=C12)C1=CC2=CC=C(C=C2N=C1N)N1CCC(CC1)C1=CC=NC=C1
31% @ 62 nM
Reading: Replacing 4-cyano with 4-(pyridin-4-yl) on the piperidine extends into a polar pocket and boosts low-dose potency by ~12 percentage points, while keeping CLogP comfortably under 5.5 and TPSA below 60 Ų.
Similarity 0.95 Δ Inhibition 0.9% Cliff 4 — para-Br vs unsubstituted phenyl on thiazole
LMK-5-66 (4-Br-Ph)
CN(C)C1=CC=C2C=C(C3=NC(=CS3)C3=CC=C(Br)C=C3)C(N)=NC2=C1
98.9% @ 3 µM
LMK-5-67 (Ph)
CN(C)C1=CC=C2C=C(C3=NC(=CS3)C3=CC=CC=C3)C(N)=NC2=C1
99.8% @ 3 µM
Reading: Removing the bromine costs essentially zero potency at 3 µM and likely improves the metabolic profile (no halogen-mediated CYP liability). At 1 µM the gap widens (LMK-5-66 drops to 45%, LMK-5-67 still 97%), reinforcing the unsubstituted phenyl as the better R1.
Combination Bliss synergy 10.56 Cliff 5 — ISQ-1 alone vs ISQ-1 + BI2536 (Plk1 inhibitor) · the patent's headline claim
ISQ-1 alone
CN(C)C1=CC=C2C=C(C3=CN(C)C4=CC=CC=C34)C(N)=NC2=C1
~38% @ 250 nM
ISQ-1 + BI2536
co-dosed: ISQ-1 (50–400 nM) × BI2536 (1–6 nM)
Bliss 10.56 synergy
Reading: The patent's central therapeutic claim — ISQ + Plk1 inhibitor synergy in c-MYC-driven cancers — surfaces directly as the dataset's largest activity cliff. ISQ-1 alone is moderate at 250 nM, but combined with BI2536 the response crosses the +5 Bliss synergy threshold by a clear margin.
Section 06 · Discussion & takeaways

What this dataset means for an ISQ-class program.

A short reading of the chemistry, the SAR, and the open questions the patent leaves on the table.

Read end to end, US20240300921A1 reads less like a tour of medicinal-chemistry possibility space and more like a focused defense of a single combination claim. The 2-aminoquinoline scaffold is fixed across all 40 analogs; the chemistry exploration is concentrated at two positions; and the most differentiated readout in the entire dataset is not a single-agent IC50 but the Bliss synergy between ISQ-1 and a Plk1 inhibitor.

For a program looking to build on this disclosure, three observations are worth flagging:

  1. Single-agent potency saturates quickly. Roughly half the library exceeds 90% inhibition at 3 µM, which means that 3 µM is a poorly discriminating screening dose. The interesting separation happens at 250–500 nM, where the ISQ-7/8/9/10 sub-series and ISQ-3 pull away from the rest. Future SAR triage should set screening doses at this lower range.
  2. The Plk1 combination is the IP. The strongest empirical signal in the patent is the synergy with BI2536. A program that develops the single-agent without the combination story risks duplicating an already-disclosed chemotype without claiming the differentiated mechanism.
  3. Two compounds carry mutagenicity flags that are easy to fix. LMK-5-62 and LMK-5-68 both contain a p-methoxy benzothiazole. Switching to phenyl-thiazole (as in LMK-5-67) preserves > 98% inhibition while removing the structural alert — a near-free win for any de-risking exercise.

The dataset also leaves two open questions the patent does not answer. First, only one cell line (LS174T) is tested — selectivity over non-c-MYC-driven CRC lines is asserted but not shown in the SAR table. Second, the dose-response data is partial: only ISQ-2, ISQ-7, ISQ-8, ISQ-9, ISQ-10, LMK-6-89, LMK-6-99 and a handful of others have full 4-point curves. Filling these gaps is a natural next step for any team building on this chemistry.

The most actionable insight from this patent is not which compound is best — it is that the patent's commercial claim is the combination, and the SAR data backs that up.
Section 07 · FAQ

Frequently asked questions about US20240300921A1.

What is the lead compound in patent US20240300921A1?

The patent does not nominate a single lead, but the ISQ-1 compound code (1-methylindole-substituted 2-aminoquinoline with N(Me)2 at quinoline-7) is the most thoroughly profiled and is used as the partner in the BI2536 synergy study. LMK-5-67 (phenyl-thiazole + N(Me)2) is the most potent single agent at 99.8% inhibition @ 3 µM.

What cell line is the SAR run against?

All 95 records were generated against the LS174T human colon adenocarcinoma cell line — a c-MYC-driven CRC model frequently used to evaluate compounds targeting the c-MYC pathway. The endpoint is cell-proliferation inhibition over a 5-day exposure, dosed via culture-medium addition.

Why does the patent emphasize a Plk1 combination?

Polo-like kinase 1 (Plk1) is a downstream effector linked to c-MYC-driven proliferation. The patent reports that co-dosing the lead compound ISQ-1 with the clinical Plk1 inhibitor BI2536 produces a Bliss synergy score of 10.56 against LS174T — well above the +5 threshold conventionally used to distinguish synergy from additivity.

Are any of the disclosed compounds flagged for safety liabilities?

Yes. Two compounds — LMK-5-62 and LMK-5-68 — return a high mutagenicity flag in the in-silico Ames model. Both share a p-methoxy benzothiazole R1 group, a known structural alert. The remaining 38 compounds return no flags.

Where does the SAR data on this page come from?

The 95 activity records are extracted from Table 3 (page 31) of patent US20240300921A1 by the Eureka LS extraction engine. Multi-dimensional descriptors and the 211 activity-cliff pairs are computed automatically using standard cheminformatics methods.

Can I extract SAR data from any patent like this?

Yes — Eureka LS supports patents from USPTO, EPO, WIPO and CNIPA, either by patent number or PDF upload. The extraction engine generates a structured SAR table, the multi-dimensional descriptor profile, and activity-cliff comparisons in under 30 seconds. Try it on your patent of interest →

Section 08 · References

Where the data comes from.

  1. Patent US20240300921A1 — "Indole-substituted quinolines and their combination with Plk1 inhibitors for the treatment of cancer." Filed at the USPTO; activity data sourced from Table 3, page 31. https://patents.uspto.gov/patent/US20240300921A1
  2. Eureka LS SAR extraction engine — Auto-extracted compound table, dosing regimen, SMILES, and synergy data from the patent PDF. https://eureka.patsnap.com/ls/#/home/sar
  3. Eureka LS Multi-dimensional Overview — CLogP, TPSA, druglikeness, ligand efficiency, mutagenicity, scaffold and ring decomposition computed via standard cheminformatics methods.
  4. Eureka LS Activity Cliff Comparison — 211 pairwise comparisons of structural similarity (Tanimoto on Morgan fingerprints) and activity delta across the 40-compound library.
  5. BI2536 — Reference Plk1 inhibitor used in the patent's combination study. Steegmaier et al., Curr Biol 2007, 17(4): 316–322.
Free plan available · No credit card required

Stop reading patents. Start extracting SAR.

Eureka LS turns any pharmaceutical patent into a structured SAR dataset, multi-dimensional descriptor profile, and activity-cliff map — in under 30 seconds.

5 free extractions / month USPTO · EPO · CNIPA · WIPO CSV / XLSX / SDF export Multi-dimensional Overview & Activity Cliff