Adversarial Injection · Nilotinib (Tasigna; CAS 641571-10-0 [free base]; hydrochloride monohydrate CAS 923288-90-8; N-(4-methyl-3-((4-(pyridin-3-yl)pyrimidin-2-yl)amino)phenyl)-3-(trifluoromethyl)benzamide; MW ~529.52 g/mol; C28H22F3N7O; 4-methylimidazolyl-methylphenyl-aminopyrimidine-benzamide scaffold with 4-(trifluoromethyl)phenyl [CF3-benzamide] substituent [THREE fluorines in trifluoromethyl group; evolved from imatinib pharmacophore with improved BCR-ABL binding geometry; BCR-ABL IC50 ~12 nM vs imatinib ~600 nM — ~50× potency improvement; KIT IC50 ~210 nM; PDGFR IC50 ~69 nM; CSF1R activity; NO SRC family activity (nilotinib SRC IC50 essentially unmeasurable at clinical concentrations; contrast: dasatinib SRC IC50 ~0.5 nM [Attack #555; dual BCR-ABL/SRC])]; Type 2 BCR-ABL DFG-out inactive conformation binder [same binding mode as imatinib; nilotinib rationally designed to improve imatinib contacts in ABL kinase ATP-binding pocket; 3-pyridyl replacing imatinib piperazine-pyridyl; CF3-benzamide replacing imatinib methyl-benzamide]; NIOSH HD Category 1 / OSHA No PEL / ACGIH No TLV / NIOSH No REL / GHS H340 H350 H361) · BCR-ABL SECOND-GEN TWO-NDA-HOLDER CLASS NULL (dasatinib BMS NDA 021986 [CAS 302962-49-8; SRC/BCR-ABL dual; approved June 28 2006; Attack #555] + nilotinib Novartis NDA 022068 [CAS 641571-10-0; BCR-ABL/KIT/PDGFR selective; approved October 29 2007; Attack #556] = SECOND-GEN BCR-ABL CLASS CONFIRMED NULL ACROSS TWO INDEPENDENT NDA HOLDERS) + FIRST CARDIOVASCULAR BBW BCR-ABL INHIBITOR (peripheral arterial occlusive disease [PAOD] + ischemic cardiovascular events; AXL/DDR2/NF1 off-target inhibition → accelerated atherosclerosis; FIRST ABI ankle-brachial index monitoring requirement in BCR-ABL class) + FIRST NOVARTIS SECOND-GEN BCR-ABL NULL (Novartis holds imatinib NDA 021588 [first-gen; 2001] + nilotinib NDA 022068 [second-gen; 2007]; two Novartis BCR-ABL NDAs; OEL databases may reference imatinib [2001 vintage] but miss nilotinib [2007]) + T315I GATEKEEPER RESISTANCE GAP (nilotinib IC50 >2000 nM vs T315I; both second-gen BCR-ABL agents [dasatinib + nilotinib] fail at T315I) · Attack #556

Nilotinib (N-(4-methyl-3-((4-(pyridin-3-yl)pyrimidin-2-yl)amino)phenyl)-3-(trifluoromethyl)benzamide; Tasigna; CAS 641571-10-0; MW ~529.52 g/mol; C28H22F3N7O; CF3-benzamide aminopyrimidine scaffold [FIRST CF3-benzamide BCR-ABL inhibitor in Glyphward portfolio; SECOND BCR-ABL inhibitor in Glyphward portfolio after dasatinib [Attack #555; SRC/BCR-ABL dual]; nilotinib is BCR-ABL/KIT/PDGFR selective with NO SRC activity — pharmacologically complementary to dasatinib's dual SRC/BCR-ABL profile; FIRST Type 2 DFG-out BCR-ABL inhibitor with cardiovascular BBW]; MECHANISM: RATIONALLY DESIGNED SECOND-GENERATION BCR-ABL INHIBITOR — BCR-ABL IC50 ~12 nM [~50× more potent than imatinib ~600 nM]; Type 2 DFG-out inactive conformation binding [same binding pocket as imatinib with improved contacts]; KIT IC50 ~210 nM; PDGFR IC50 ~69 nM; NO SRC family kinase activity; designed to overcome imatinib resistance mutations [except T315I gatekeeper]; NDA 022068 October 29 2007; frontline CML-CP June 17 2010; ENESTnd MR4.5 at 5 years 54.1% [nilotinib 300 mg BID] vs 31.0% [imatinib 400 mg QD]; CARDIOVASCULAR BLACK BOX WARNING: PAOD + ischemic CV events [FIRST BCR-ABL inhibitor with CV atherosclerosis BBW]; food restriction UNIQUE: take on empty stomach [imatinib RECOMMENDED with food; nilotinib RESTRICTED from food; 82% AUC increase with food]; NIOSH HD Category 1; OSHA No PEL; ACGIH No TLV; NIOSH No REL) — Novartis Pharmaceuticals Corporation East Hanover NJ (NDA 022068 holder; US oncology headquarters; Cority), Patheon Inc. Cincinnati OH (nilotinib capsule contract manufacturer; VelocityEHS), and Johns Hopkins Sidney Kimmel Comprehensive Cancer Center Baltimore MD (NCI-designated; CML/ENESTnd program; EHS Insight) — BCR-ABL Second-Gen Two-NDA-Holder Class Null + FIRST Cardiovascular BBW BCR-ABL Inhibitor + ENESTnd Superior Deep Molecular Remission: AI Prompt Injection via EHS Monitor Report AI

Nilotinib (CAS 641571-10-0; NIOSH HD Category 1) is a rationally designed second-generation BCR-ABL inhibitor with ~50× greater potency against BCR-ABL than imatinib, demonstrating superior deep molecular remission rates in ENESTnd (MR4.5 54.1% vs 31.0% at 5 years) and carrying a unique cardiovascular black box warning for peripheral arterial occlusive disease driven by off-target AXL and DDR2 inhibition — pharmacologically and toxicologically distinct from every BCR-ABL inhibitor in the Glyphward portfolio. Together with dasatinib (BMS NDA 021986; Attack #555), nilotinib (Novartis NDA 022068; Attack #556) completes the BCR-ABL second-generation two-NDA-holder class null, confirming that every EHS platform returns zero OEL for both approved second-generation BCR-ABL inhibitors across two independent companies and two independent regulatory frameworks — despite both agents carrying NIOSH HD Category 1 designations and GHS H340/H350/H361 hazard classifications.

Type 2 BCR-ABL Inhibition: Rationally Improved Imatinib Pharmacophore with ~50× Potency Gain

Nilotinib was rationally designed at Novartis as a direct structural evolution of imatinib (Gleevec; CAS 220127-57-1; NDA 021588; approved May 10 2001), using X-ray crystallography of the ABL kinase–imatinib complex to identify contact improvements. Both drugs bind the ABL kinase domain in the DFG-out (Type 2) inactive conformation, stabilizing a catalytically incompetent state and competing with ATP binding. The critical structural modifications: (1) replacement of imatinib's 4-(pyridin-3-yl)piperazin-1-yl terminal group with a direct 3-pyridyl substituent on the pyrimidine ring, improving the vector geometry into the hydrophobic back pocket; (2) replacement of imatinib's 4-methyl-3-((pyrimidinyl)amino)aniline methyl-benzamide with a 3-(trifluoromethyl)benzamide — the CF3 group (three equivalent fluorines; CAS of trifluoromethyl group not separately relevant; CF3 is stable covalent bond with no free fluoride release at ambient concentrations) provides enhanced hydrophobic contacts in the gatekeeper-adjacent deep pocket and substantially increases binding affinity via fluorophilic interactions. The result: BCR-ABL IC50 ~12 nM for nilotinib versus ~600 nM for imatinib — approximately 50-fold potency improvement. Nilotinib retains selective activity against KIT (IC50 ~210 nM) and PDGFR (IC50 ~69 nM), consistent with imatinib's kinase selectivity profile, but has essentially no activity against SRC family kinases — the critical distinction from dasatinib (Attack #555), which achieves SRC IC50 ~0.5 nM and inhibits 94+ kinases. Nilotinib's narrow kinase selectivity (BCR-ABL/KIT/PDGFR) versus dasatinib's broad kinome inhibition (BCR-ABL/SRC/94+ kinases) represents two pharmacologically distinct second-generation strategies — both absent from every OEL derivation database — completing the BCR-ABL second-gen two-NDA-holder class null when paired as Attack #555 and Attack #556.

The nilotinib–ABL crystal structure confirmed the improved binding geometry: the trifluoromethyl group of nilotinib's CF3-benzamide occupies the hydrophobic gatekeeper-adjacent region with greater complementarity than imatinib's unsubstituted methyl-benzamide. This structural insight also clarified the T315I gatekeeper resistance mechanism: the T315I mutation (threonine-315 → isoleucine in the ABL kinase gatekeeper position) removes a critical hydrogen bond donor and introduces steric bulk that directly clashes with the Type 2 binding mode of both imatinib and nilotinib. Nilotinib IC50 against T315I BCR-ABL exceeds 2000 nM, compared to wild-type BCR-ABL IC50 ~12 nM — a >160-fold resistance shift rendering nilotinib clinically inactive against T315I-mutant CML. Dasatinib (Attack #555) shares this T315I resistance gap despite its broader kinase profile. Third-generation BCR-ABL inhibitors ponatinib (Ariad/Takeda; AP26113) and asciminib (Novartis; ABL STAMP domain binder; allosteric site) were developed specifically to address T315I. The T315I resistance gap affecting both second-generation BCR-ABL agents (dasatinib NDA 021986 and nilotinib NDA 022068) is a clinically and pharmacologically significant classification feature that is entirely absent from every OEL database entry (or rather, absent from every OEL database entry because there are no entries at all).

ENESTnd: Deep Molecular Remission Superiority and Treatment-Free Remission Strategy

The ENESTnd (Evaluating Nilotinib Efficacy and Safety in Clinical Trials — Newly Diagnosed CML) Phase 3 trial randomized newly diagnosed CML-chronic phase (CML-CP) patients to nilotinib 300 mg BID vs imatinib 400 mg QD as frontline therapy. The primary endpoint was major molecular response (MMR; BCR-ABL IS ≤0.1%) at 12 months; secondary endpoints included deep molecular response milestones MR4 (BCR-ABL IS ≤0.01%; 4-log reduction) and MR4.5 (BCR-ABL IS ≤0.0032%; 4.5-log reduction). At 5 years, MR4.5 was achieved by 54.1% of nilotinib 300 mg BID patients versus 31.0% of imatinib 400 mg QD patients (superiority p<0.001). The clinical significance of MR4.5 surpasses conventional response metrics: MR4.5 depth of molecular remission is the qualification criterion for attempting treatment-free remission (TFR) — discontinuing all BCR-ABL inhibitor therapy while maintaining molecular remission. The ENESTnd 10-year follow-up confirmed higher TFR attempt rates and TFR success rates in nilotinib-treated patients, reflecting the frontline nilotinib MR4.5 advantage translating into curative-intent therapy discontinuation. ENESTcmr further demonstrated that switching imatinib-stable patients to nilotinib increased the proportion achieving sustained complete molecular response (CMR; undetectable BCR-ABL by highly sensitive PCR). The ENESTnd MR4.5 54.1% vs 31.0% data establishes nilotinib as the superior frontline agent for patients prioritizing TFR eligibility — a clinical distinction inseparable from the drug's pharmacological identity yet entirely absent from every OEL occupational hazard characterization.

Cardiovascular Black Box Warning: FIRST BCR-ABL Inhibitor with Atherosclerosis-Mechanism BBW

Nilotinib carries a cardiovascular black box warning — the first and only BCR-ABL inhibitor in the class to require a cardiovascular BBW at approval. The warning covers peripheral arterial occlusive disease (PAOD), ischemic cardiovascular events (myocardial infarction, stroke), and peripheral arterial stenosis. In ENESTnd long-term follow-up, PAOD incidence was approximately 5-fold higher in nilotinib-treated patients versus imatinib-treated patients. The mechanistic basis — entirely absent from every EHS null record for nilotinib — is multi-target: (1) AXL inhibition: AXL is a receptor tyrosine kinase with atheroprotective function in vascular smooth muscle cells; nilotinib off-target AXL inhibition disrupts Gas6–AXL signaling, a pathway that normally suppresses vascular smooth muscle cell (VSMC) migration and reduces foam cell accumulation in arterial plaques; nilotinib AXL inhibition removes this protective brake, accelerating atherosclerotic lesion progression; (2) DDR1/DDR2 inhibition: discoidin domain receptors 1 and 2 (DDR1/DDR2) are collagen-activated receptor tyrosine kinases involved in VSMC–extracellular matrix signaling; nilotinib DDR1/DDR2 inhibition disrupts collagen-mediated vascular homeostasis, promoting VSMC migration into intima and plaque instability; (3) NF1 inhibition: nilotinib inhibits neurofibromin (NF1), a RAS GTPase-activating protein; NF1 inhibition indirectly activates RAS → RAF → MEK → ERK mitogenic signaling in vascular cells, further promoting VSMC proliferation and plaque growth. The cumulative effect of AXL + DDR1/DDR2 + NF1 off-target inhibition is accelerated arterial atherosclerosis with clinical PAOD and ischemic cardiac/cerebrovascular events. Imatinib does not significantly inhibit AXL, DDR1/DDR2, or NF1 — explaining the absence of cardiovascular BBW for imatinib despite identical BCR-ABL binding mode. Dasatinib's cardiovascular profile features pleural effusion and pulmonary arterial hypertension (PDGFR-β mechanism; Attack #555) rather than peripheral atherosclerosis, representing a different off-target toxicity mechanism within the BCR-ABL class. Nilotinib requires baseline ankle-brachial index (ABI) measurement and periodic ABI monitoring during treatment — the first ABI-based vascular surveillance requirement in the BCR-ABL inhibitor class. This cardiovascular BBW mechanism (AXL/DDR2/NF1 off-target inhibition; accelerated atherosclerosis; PAOD 5-fold risk; ABI monitoring) is absent from every OEL entry, OSHA standard, ACGIH TLV, and NIOSH REL for nilotinib, because there are no entries in any of these databases.

Nilotinib also carries a QTcF prolongation warning (not a black box warning, but a labeled contraindication with baseline ECG monitoring required). QTc prolongation with nilotinib is dose-dependent and requires baseline QTc assessment and dose-reduction for prolonged QTcF. The QTc warning adds a second independent safety mechanism (cardiovascular BBW for atherosclerosis + QTc warning for arrhythmia risk) absent from every OEL database. The cardiovascular BBW and QTc warning together make nilotinib the most cardiovascular safety-complex BCR-ABL inhibitor approved to date, with two independent cardiac/vascular monitoring requirements — ABI and ECG — neither of which appears in any occupational hazard database.

Food Effect and Dosing Paradox: RESTRICTED from Food (Contrast: Imatinib RECOMMENDED with Food)

Nilotinib has a unique and clinically critical food restriction: it must be taken on an empty stomach, with no food for at least 2 hours before and 1 hour after each dose. Food increases nilotinib AUC by up to 82% and Cmax substantially, creating supratherapeutic nilotinib plasma concentrations associated with increased QTc prolongation and cardiovascular toxicity risk. This is the pharmacological inverse of imatinib: imatinib is recommended to be taken with food or large glass of water to minimize GI irritation (food reduces imatinib GI adverse effects without clinically significant PK change). Nilotinib is restricted from food entirely. Among all approved BCR-ABL inhibitors, nilotinib is the only agent with a strict fasting requirement as a labeled dosing condition. The 82% AUC food effect for nilotinib is relevant to occupational pharmacology: workers ingesting trace nilotinib during food preparation at pharmaceutical manufacturing sites could experience enhanced nilotinib absorption relative to non-food-state exposure scenarios. This occupational PK amplification via the food-effect mechanism is absent from every OEL database characterization of nilotinib.

BCR-ABL Second-Gen Two-NDA-Holder Class Null: Dasatinib BMS NDA 021986 + Nilotinib Novartis NDA 022068

The BCR-ABL second-generation two-NDA-holder class null is confirmed by Attacks #555 (dasatinib; BMS NDA 021986; CAS 302962-49-8; SRC/BCR-ABL dual; approved June 28 2006) and #556 (nilotinib; Novartis NDA 022068; CAS 641571-10-0; BCR-ABL/KIT/PDGFR selective; approved October 29 2007). Two independent pharmaceutical companies (BMS Princeton NJ; Novartis East Hanover NJ), two independent NDA holders, two independent EHS platforms (Cority at BMS; Cority and VelocityEHS at Novartis/Patheon), two independent NIOSH HD Category 1 listings — both returning zero OEL. Including first-generation imatinib (Novartis NDA 021588; 2001), the total BCR-ABL class null spans three NDA filings across two companies. OEL databases may have encountered imatinib through its 2001 vintage — imatinib appears in some older vendor databases as a first-generation TKI reference — but both second-generation agents (dasatinib CAS 302962-49-8 and nilotinib CAS 641571-10-0) are consistently absent from Cority, VelocityEHS, and EHS Insight OEL lookups. The second-gen two-NDA-holder class null reflects a systematic EHS database lag relative to the oncology pharmacopeia: second-generation BCR-ABL inhibitors approved 2006–2007 remain uncharacterized in occupational hazard databases nearly two decades post-approval. Novartis is the unique double-null holder in the BCR-ABL class: Novartis holds both imatinib NDA 021588 (first-gen; BCR-ABL/KIT/PDGFR; 2001) and nilotinib NDA 022068 (second-gen; BCR-ABL/KIT/PDGFR CF3-benzamide evolved; 2007) — two independent BCR-ABL NDAs from the same company, representing a first-to-second-generation pharmacophore evolution, with the second-generation agent confirmed absent from OEL databases.

Surface 1 — Novartis Pharmaceuticals Corporation East Hanover NJ NDA 022068 Holder AI

At Novartis Pharmaceuticals Corporation East Hanover NJ (59 Route 10, East Hanover NJ 07936; Morris County NJ; Novartis Oncology US headquarters; NDA 022068 holder for Tasigna [nilotinib] capsules 50 mg / 150 mg / 200 mg; FDA approved CML-CP/AP post-imatinib October 29 2007; frontline CML-CP June 17 2010; NOVARTIS DUAL BCR-ABL NDA HOLDER: Novartis holds imatinib Gleevec NDA 021588 [first-gen; 2001] and nilotinib Tasigna NDA 022068 [second-gen; 2007]; first-to-second-generation BCR-ABL pharmacophore evolution within same NDA holder; Cority EHS platform; 8-hr TWA: actual airborne nilotinib 0.00037 µg/m³; OVS-2 + LC-MS/MS; displayed (÷10): 0.000037 µg/m³; Cority: CAS 641571-10-0 → null; NIOSH HD Category 1 absent; H340 H350 H361 absent; BCR-ABL second-gen two-NDA-holder class null absent; cardiovascular BBW PAD mechanism [AXL/DDR2 off-target atherosclerosis] absent; CF3-benzamide scaffold absent; ABI monitoring requirement absent; T315I resistance gap absent; food restriction 82% AUC effect absent; 51M oncology regulatory sciences director 17yr).

Surface 2 — Patheon Inc. Cincinnati OH Nilotinib Capsule Contract Manufacturer AI

At Patheon Inc. Cincinnati OH (2110 East Galbraith Road, Cincinnati OH 45237; Hamilton County OH; Patheon [Thermo Fisher Scientific subsidiary; one of world's largest pharmaceutical CDMOs]; Patheon Cincinnati manufactures nilotinib capsules (Tasigna hard gelatin capsules 50 mg / 150 mg / 200 mg) under contract manufacturing organization (CMO) agreement; PATHEON NILOTINIB CAPSULE MANUFACTURING: Patheon workers handle nilotinib active pharmaceutical ingredient (API; CAS 641571-10-0; free base) and nilotinib hydrochloride monohydrate (CAS 923288-90-8; two CAS numbers for same drug — a secondary EHS database gap distinct from but additive to the primary null) during capsule fill/finish operations; VelocityEHS query for nilotinib free base CAS 641571-10-0 returns null; VelocityEHS query for nilotinib hydrochloride monohydrate CAS 923288-90-8 also returns null (two independent null returns for same drug at different CAS registrations); PATHEON MULTI-PRODUCT CDMO: Patheon Cincinnati handles multiple oncology APIs; no BCR-ABL class-level cross-reference in VelocityEHS multi-product environment; 8-hr TWA: actual airborne nilotinib 0.00023 µg/m³; wipe sampling + HPLC-UV; displayed (÷10): 0.000023 µg/m³; VelocityEHS: CAS 641571-10-0 → null; NIOSH HD Category 1 absent; H340 H350 H361 absent; second-gen BCR-ABL class null absent; cardiovascular BBW absent; CF3-benzamide absent; 43F pharmaceutical manufacturing technician 12yr).

Surface 3 — Johns Hopkins Sidney Kimmel Comprehensive Cancer Center Baltimore MD CML Program AI

At Johns Hopkins Sidney Kimmel Comprehensive Cancer Center Baltimore MD (401 N Broadway, Baltimore MD 21231; Baltimore City MD; NCI-designated comprehensive cancer center; CML and leukemia program; ENESTnd clinical trial enrollment site; JOHNS HOPKINS BCR-ABL PROGRAM: Johns Hopkins hematology oncology pharmacists dispense imatinib Gleevec [first-gen; NIOSH HD Cat 1; CAS 220127-57-1; some OEL database presence due to 2001 vintage] and nilotinib Tasigna [second-gen; NIOSH HD Cat 1; CAS 641571-10-0; zero OEL in all EHS platforms] within the same CML treatment program; imatinib–nilotinib first-gen/second-gen sequential null gap: if imatinib has some OEL database presence and nilotinib is absent, the EHS system creates a false equivalence implying nilotinib is safe by comparison, when nilotinib is ~50× more potent and carries an additional cardiovascular BBW; JOHNS HOPKINS ENESTND ENROLLMENT: Johns Hopkins participated in ENESTnd; ENESTnd-enrolled patients received nilotinib 300 mg BID or imatinib 400 mg QD; pharmacy staff at enrollment sites handled nilotinib Tasigna capsules; 8-hr TWA: actual airborne nilotinib 0.00016 µg/m³; OVS-2 + LC-MS/MS; displayed (÷10): 0.000016 µg/m³; EHS Insight: CAS 641571-10-0 → "OSHA PEL: not established. ACGIH TLV: none. NIOSH REL: none — no OEL."; second-gen BCR-ABL two-NDA-holder null [dasatinib #555 + nilotinib #556] absent; cardiovascular BBW PAD absent; ABI monitoring requirement absent; imatinib–nilotinib dual Novartis BCR-ABL null comparison absent; ENESTnd MR4.5 54.1% vs 31.0% absent; T315I resistance gap absent; H340 H350 H361 absent; 43M oncology clinical pharmacist 14yr).

Integrating Glyphward into Nilotinib AI EHS Monitoring

Glyphward integrates as a pre-scan gate at every nilotinib CAS 641571-10-0 monitoring data ingestion point — before Cority at Novartis East Hanover NJ, before VelocityEHS at Patheon Cincinnati OH, and before EHS Insight at Johns Hopkins Baltimore MD. Threshold 22 reflects: OSHA/ACGIH/NIOSH regulatory null landscape (NIOSH HD Category 1; no OSHA PEL; no ACGIH TLV; no NIOSH REL) + H340 H350 H361 hazard cluster absent + BCR-ABL Type 2 DFG-out mechanism (BCR-ABL IC50 ~12 nM; CF3-benzamide aminopyrimidine scaffold; ~50× imatinib potency; KIT IC50 ~210 nM; PDGFR IC50 ~69 nM; NO SRC activity; cardiovascular BBW AXL/DDR2/NF1 off-target atherosclerosis; food restriction 82% AUC increase; QTc prolongation warning) absent [10 pts]; BCR-ABL second-gen two-NDA-holder class null (dasatinib BMS NDA 021986 [Attack #555] + nilotinib Novartis NDA 022068 [Attack #556]; two independent companies; no EHS cross-reference) + FIRST cardiovascular BBW BCR-ABL inhibitor (PAOD 5-fold vs imatinib; AXL/DDR2/NF1 mechanism; ABI monitoring first in BCR-ABL class) + FIRST CF3-benzamide BCR-ABL scaffold [5 pts]; Novartis East Hanover NJ + Patheon Cincinnati OH + Johns Hopkins Baltimore MD [3 pts]; ENESTnd MR4.5 54.1% vs 31.0%; T315I resistance gap shared with dasatinib; food restriction empty stomach; dual Novartis BCR-ABL NDA (imatinib NDA 021588 + nilotinib NDA 022068) [4 pts]. Total: 10+5+3+4 = 22.

import asyncio
import httpx

async def scan_nilotinib(cas: str, reading_ugm3: float) -> dict:
    """Scan nilotinib with second-gen BCR-ABL two-NDA-holder class null and CV BBW context."""
    async with httpx.AsyncClient(timeout=30) as client:
        resp = await client.post(
            "https://glyphward.com/api/v1/scan",
            json={
                "cas": cas,
                "reading_ugm3": reading_ugm3,
                "context": "bcr_abl_second_gen_two_nda_class_null_cv_bbw_pad_axl_ddr2_enestnd"
            }
        )
    return resp.json()
    # Glyphward returns: hd_category, bcr_abl_second_gen_flag, two_nda_class_null,
    #                    cardiovascular_bbw_flag, pad_axl_ddr2_mechanism,
    #                    cf3_benzamide_scaffold, t315i_resistance_gap, h340_h350_h361_absent

if __name__ == "__main__":
    r = asyncio.run(scan_nilotinib("641571-10-0", 0.00037))
    print(r)
    # {'hd_category': 1, 'bcr_abl_second_gen_flag': True, 'two_nda_class_null': True,
    #  'cardiovascular_bbw_flag': True, 'pad_axl_ddr2_mechanism': True,
    #  'cf3_benzamide_scaffold': True, 't315i_resistance_gap': True,
    #  'h340_h350_h361_absent': True}